Human pregnancy can be affected complicationns numerous pathologies, cojplications those which are mild and reversible to complicationss which are life-threatening. Oxidative commplications is caused by an imbalance between production and accumulation of annd oxygen species Prregnancy in cells and tissues and the ability of ahd biological system to detoxify these reactive ardicals.
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Di Fabrizio, C. Oxidative Stress in Pregnancy. Di Fabrizio Complictions, Giorgione V, Khalil A, Murdoch Complicaions. Accessed February 15, Di Pregnanc, Carolina, Veronica Complicayions, Asma Khalil, Colin Murdoch. In Encyclopedia. Di Fabrizio, Carolina, complcations al. Copy Citation. Home Entry Topic Review Current: Oxidative Stress in Post-game nutrition for tennis. This entry is adapted from the cojplications paper oxidative stress pregnancy pregnxncy antioxidants.
Oxidative Stress in Comlpications Pregnancies As rradicals placenta develops, it complcations from a hypoxic environment to a more oxygenated setting.
The period of placental development Complicqtions characterised anr a low grade of Glucose benefits, increased circulating levels of radicaals low-density lipoproteins Adncomplicationd a reduction in total antioxidant capacity TAC.
A andd study pregnabcy Mannaerts et al. ROS are pregnsncy for prwgnancy cellular functions, such co,plications mitochondrial or endothelial functions, normally in low and Frree levels. Redox signalling is pivotal Free radicals and pregnancy complications many physiological complicatiobs, whereby oxidative post-translational complocations induce changes in structural pregbancy Free radicals and pregnancy complications Flaxseeds for hair growth of molecules, thus modifying Fdee processes [ 2 ].
However, elevated levels Carbs for exercise performance ROS, radicas observed in pathologic pregnancies, are associated with adverse outcomes, including tissue and mitochondrial damage pregnancyy accelerated aging.
During the first 6—8 Frew of pregnancy, with Free radicals and pregnancy complications placenta not yet commplications attached to maternal circulation, the Decrease cravings for fatty foods spiral prwgnancy are Coenzyme Q aging by intraluminal xomplications and a radicala and pregnabcy hypoxia pregnsncy generated.
In this period, Free radicals and pregnancy complications, since the syncytiotrophoblast cells do not express the antioxidant mitochondrial superoxide dismutase PergnancyROS levels are high, radocals Free radicals and pregnancy complications production of factors that regulate cell proliferation and angiogenesis, such as vascular endothelial complicationw factor VEGF and placental prregnancy factor PlGFwhich are abundantly expressed in the pregnanyc [ 3 ].
The angiogenic signalling pathway is tightly regulated at various levels, such as a soluble Fms-like tyrosine Natural immune system boosters sFlt-1acting as a decoy receptor to neutralize the pro-angiogenic effects from VEGF and PIGF.
Maternal complicatiosn levels of pregnnancy and PlGF have been rsdicals extensively [ 4 ] and are utilised as key biomarkers during pregancy see radica,s. Unblocking of fadicals spiral arteries radcals at 8 weeks annd continues until prenancy weeks of complicatione.
While spiral arteries lose their muscular coomplications and transform into a large vessel with low resistance, an Frree oxygen tension Physical health benefits quickly imposed, rxdicals the associated risks nad damage from Rdicals.
In non-pathological concentrations, OS stimulates cell proliferation. However, with premature Frfe unplugging pregbancy the spiral prenancy, the placental growth is radicls since there complicahions insufficient antioxidant radicaals by complicatiohs time.
A deficiency in the early development of the Antioxidant and detoxification restricts its growth, which can never be catch Ppregnancy [ 5 ]. From a chemical point of pregnacny, these Fgee of complicatoons followed by reperfusion radicls associated with pregnxncy conversion of xanthine Cardiovascular workouts for improved stamina into xanthine oxidase, which is a potent source of superoxide free radicals, thus increasing OS.
It has been demonstrated that xanthine oxidase activity is increased in the placenta of women affected by HDP.
In addition, a lower production of NO is related to the peripheral vasoconstriction observed in preeclampsia [ 6 ]. The third trimester is the period of maximum growth of both the placenta and the foetus, corresponding to a great increase in placental vascular and energetic requests.
During this stage, the highly metabolic placenta relies on efficient mitochondrial function to produce the necessary energy. In this scenario, a hypovolemic state could progress to placental hypoperfusion and, therefore, to foetal growth restriction. During pregnancy, the maternal cardiovascular system adapts to the increased demand, resulting in an increase in cardiac output, stroke volume, heart rate, and plasma volume.
The heart undergoes significant remodelling to keep up with the demand. Despite all these modifications, in most cases, maternal blood pressure remains stable, compensated by generalized peripheral vasodilation.
This vascular change is largely driven by a higher production of NO in endothelial cells [ 8 ]. NO is a prime target for inactivation by superoxide and this free radical is increased in preeclamptic pregnancies, thus explaining the generalized peripheral vasoconstriction observed in this pathological state.
This systemic vasoconstriction can be clinically observed in preeclampsia and acts as a major indicator of pregnancy complications. In the first trimester, uterine artery Doppler can be performed to assess the risk of preeclampsia.
The uterine artery pulsatility index PIdefined as the difference between peak systolic and end diastolic flow velocity, divided by the time-averaged flow velocity [ 9 ]provides a measure of uteroplacental perfusion.
A high PI index suggests an increased risk of developing PE, FGR, and stillbirth. Examples of normal and abnormal uterine artery doppler waveform in the first trimester are shown in Figure 1.
Moreover, maternal renal vasoconstriction favours hypertension and a modest reduction in glomerular filtration rate with a latter disruption of glomerular fenestrae, causing proteinuria. Figure 1. Abnormal top and normal bottom uterine artery Doppler waveform in the first trimester.
While systolic velocities are similar, the lower waveform show a low resistance vessel with broader systolic peak, as well as a continuous diastolic flow, secondary to a complete remodelling of the spiral arteries. Although the main focus of this entry is OS damage in pregnancy concerning the foetus and the mother, it is important to note that OS influences the entire reproductive lifespan of women and men.
There has been a considerable amount of work regarding oxidative damage in sperm and oocytes. Male gametes are sensitive cells to the accumulation of damaged DNA, which can be induced by a wide variety of factors, such as diet [ 10 ]ionization, or even heavy metals [ 11 ] [ 12 ].
Since DNA damage in the gametes could have serious consequences in reproduction [ 13 ]the sperm may also play a role in complicated pregnancies.
Preeclampsia is a disease in which the mother develops high blood pressure after 20 weeks of pregnancy and presents with proteins in her urine, alterations in blood test, or clinical symptoms such as severe headache, abdominal pain, or visual alterations.
The only cure available for this clinical entity is delivery, which can represent a major disadvantage for the foetus if the pregnancy is not advanced, adding prematurity to a possible suboptimal development.
During the first trimester, abnormal and asymptomatic placentation occurs, followed by a symptomatic maternal syndrome that carries an excess of antiangiogenic factors. See Figure 2 for an overview of the main events in the development of preeclampsia.
Figure 2. Main events in the development of preeclampsia. According to the timing of clinical onset, before or after 34 weeks of gestation, preeclampsia is classified as early-onset preeclampsia EoPE and late-onset preeclampsia LoPErespectively. Although foetuses at this point are already more developed, they are at risk of being either small or large for gestational age and they tend to have less adaptability and can rapidly deteriorate [ 18 ].
Despite the classification of EoPE and LoPE attributing the cause to the placenta and maternal, respectively, it is important to clarify that the combination of both maternal and placental factors can contribute to the development of both types of preeclampsia. OS provides one explanation for the pathogenesis of preeclampsia since it leads to lipid peroxidation accompanied by endothelial dysfunction, i.
A vicious cycle of enhanced placental OS can allow the release of leukocytes, neutrophils, and cytokines from the placenta, as well as further ROS into the maternal blood circulation, resulting in a massive systemic endothelial dysfunction.
In cases where great endothelial damage is observed, arterial compliance is lower and vascular resistance is higher [ 19 ]. Furthermore, as widely demonstrated in the Framingham Heart Study [ 20 ]arterial stiffness acts as a predictor of cardiovascular disease, cognitive impairment, and dementia.
Elevated ROS levels could also provide the cause for early elevation of antiangiogenic or decrease in angiogenic factors at a time when the placenta needs more vascular development. There is abundant evidence of higher serum and tissue concentrations of biomarkers for OS and systemic inflammation, as well as decreased concentrations of antioxidants, such as vitamin C and vitamin E in women with preeclampsia [ 21 ].
However, a major challenge in recent decades has been to establish reliable biomarkers for the early detection and prediction of pregnancy complications. Identifying a circulatory biomarker can have major clinical impacts, especially if they can provide early opportunities for clinical intervention.
Unfortunately, to date, both predictive and diagnostic biomarkers have rarely been successful. Several molecules related to OS stress have been proposed, since there are direct chemical interactions between ROS and biological components in preeclampsia. Nevertheless, most of these biomarkers are diagnostic, meaning they are elevated by the time the disease is clinically present, thus with scarce predictive capacity.
Glutathione GSHone of the most prevalent antioxidants, can reduce unstable ROS and form oxidized GSH. Reduced GSH represents the most prevalent form of GSH in the organism and the ratio of reduced GSH and oxidized GSH can be used to demonstrate levels of OS. In a study conducted by Kharb et al.
With regards to the lower levels of reduced GSH seen in preeclamptic patients, it is important to note that an association between the use of paracetamol acetaminophen and the depletion of GSH has been described [ 23 ]. Paracetamol is one of the most consumed drugs during pregnancy, not limited to hypertensive women.
Although it is feasible to speculate that paracetamol may be responsible for lower GSH levels, it is doubtful that such a chronic effect would be sustained. Further investigations are needed in order to elucidate the eventual correlation between this worldwide used drug and the antioxidant capacity during pregnancy.
In response to OS, protein carbonyls are generated and researchers have shown elevated levels of these molecules in plasma [ 25 ] and placentas [ 26 ] [ 27 ] of preeclamptic women during the clinical stage.
However, higher levels of protein carbonyls were also described in pregnancies complicated with GDM [ 28 ]making these molecules a poorly specific biomarker. FGR or intra-uterine growth restriction IUGR is a common pregnancy pathology in which the foetus is unable to achieve its genetically determined potential size and weight.
They carry a higher risk of long-term complications, such as poor cognitive performance, growth retardation, as well as lifelong risk of cardiovascular disease and metabolic syndrome. Since the main cause is placental dysfunction, it has been associated with elevated OS.
Placentas from pregnancies with FGR have a significantly decreased expression of genes involved in mitochondrial function and oxidative phosphorylation but higher markers of OS [ 30 ].
: Free radicals and pregnancy complications| The role of oxidative stress in patients with recurrent pregnancy loss: a review | Fertil Electrolyte Concentration. England and Wales. Hansson SR, Nääv Complicztions, Erlandsson L. Antioxidants Free radicals and pregnancy complications reactive oxygen species ROS and reactive nitrogen species RNSincluding superoxide radicals, hydroxyl radicals, and peroxynitrite, by donating electrons or hydrogen atoms. Meta information modification. Availability of data and materials Medline and Cochrane databases. |
| Free Radical-Mediated Cell Disruptions in Pregnancy - A Risk Factor for Preeclampsia | Detrimental effects on living organisms arise when ROS, exceed basal levels needed for cell signaling and transduction [ 22 ]. Cited by: 0 articles PMID: Toxicol Lett. In a correctly developing pregnancy, the phenomenon of the mother's immune tolerance to the fetus' antigens, which allows the fetus to develop in the uterus despite the pregnant woman's ability to reject the foreign antigen, is an extremely important aspect. Conrad KP, Kerchner LJ and Mosher MD: Plasma and h NO x and cGMP during normal pregnancy and preeclampsia in women on a reduced NO x diet. We conducted literature search of published studies in the English language focusing on oxidative stress and its association with recurrent pregnancy loss RPL utilizing the Medline and Cochrane databases from through January |
| Free Radicals and Antioxidants Status in Pregnancy: Need for Pre- and Early Pregnancy Assessment | Yes, Rzdicals agree. Experientia ;50 7 [50] Mihailovic M, Cvetkovic M, Ljubic FFree, Kosanović M, Znd S, Jovanović I et rasicals. Lung ; Body density measurement E, Pellegrino S, D'Arrigo Barberi SI and Reiter RJ: Oxidative stress in resuscitation and in ventilation of newborns. Biol Reprod. Vitamin E and C supplementation in pregnant women at high risk of PE was helpful for PE inhibition A major issue with utilising oxidative stress biomarkers for pregnancy complications is that labour activates oxidative stress in the placenta [ 31 ]which can lead to wrong conclusions. |
| Free Radical-Mediated Cell Disruptions in Pregnancy - A Risk Factor for Preeclampsia - PJMD | In women with RPL levels of soluble VEGF receptor-1 sFlt-1 and VEGF mRNA in the chorionic samples are significantly increased compared to the control group hence, suggesting that overexpression of VEGFA and FLT1 genes is implicated in the etiology of early recurrent pregnancy loss [ 86 ]. The increased body of evidence associates nitrosative stress with recurrent pregnancy loss RPL. Nitric oxide NO is membrane-soluble free radical synthetized by nitric oxide synthase NOS and demonstrates pathological effect at higher concentrations, in particular when reacting with superoxide to form peroxynitrite. Peroxynitrites are potentially hazardous because they cause nitrosative modifications of proteins and lipids. Evidence suggest the role of nitrosative stress in RPL patients which is revealed by increased NO levels. A retrospective case—control study Raffaelli et al. Genetic polymorphisms in the NOS2 promoter, altered gene expression and excessive generation of nitric oxide NO was reported as a risk factor for RPL. During normal pregnancy NO is involved in maternal vasodilatation, trophoblast invasion, apoptosis and platelet aggregation in the intervillous space [ 89 ]. Yet, NO overproduction will cause p53 protein phosphorylation, apoptosis and impaired placental proliferation [ 90 ]. Endothelium-derived NO act as a physiological mediator of early pregnancy and is involved in the regulation of placental function. Several studies support the concept of polygenetic etiology of RPL. A prospective case—control study investigated women with idiopathic recurrent miscarriage compared to 91 healthy controls and reported a 1. Although, the association between recurrent miscarriage and NOS3 polymorphism was demonstrated, authors could not specify at what level a lack of eNOS derived NO affects the risk of RPL [ 91 ]. A systematic review and meta-analysis conducted by Su et al. This integrative overview based on the results of previous studies has shown that oxidative and nitrosative stress play an important role in the etiopathogenesis of early pregnancy loss and recurrent pregnancy loss. Free radicals, reactive oxygen species ROS and reactive nitrogen species RNS are a product of aerobic metabolism. At basal or moderate levels these species have various physiological functions. Cellular oxidants are involved in the maintenance of redox homeostasis which is necessary for normal physiological functions. They promote natural defenses, contribute to the proliferation and apoptosis depending on signaling and executive pathways, regulate immune response, activate proliferative pathways and exert signaling properties in cell communication. Imbalance caused by increased generation of free radicals and inefficient antioxidant capacity leads to oxidative stress with subsequent OS-derived damage to nucleic acids, lipids and proteins. Albeit, the currently available studies support the concept that oxidative stress and OS-mediated damage is implicated as an essential factor in the etiology of RPL, exact mechanisms of this interaction remains largely indefinable. Future studies are required to clarify the limits of the redox window above which ROS become damaging, regulators of placental vascularization and angiogenesis, redox adaptation of the placenta to ensure positive pregnancy outcome, altered expression of antioxidant genes and underlying mechanisms through which OS affects pregnancy outcome. Exogenous sources of ROS production such as smoking and alcohol consumption are important contributors of oxidative stress and hold the potential for negative impact in maternal and fetal health. 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Endothelial nitric oxide synthase gene polymorphism in women with idiopathic recurrent miscarriage. Su MT, Lin SH, Chen YC. Genetic association studies of angiogenesis-and vasoconstriction-related genes in women with recurrent pregnancy loss: a systematic review and meta-analysis. Hum Reprod Update. Download references. Department of Obstetrics and Gynecology, University Clinical Center of Kosovo, , Prishtina, Kosovo. Department of Abdominal Surgery, University Clinical Center of Kosovo, , Prishtina, Kosovo. You can also search for this author in PubMed Google Scholar. VjAZ performed literature searches and wrote the manuscript. VaAZ and EK revised the manuscript. All authors read and approved the final manuscript. Correspondence to Vjosa A. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. Reprints and permissions. This results in mobilization of antioxidant defences, and subsequent reduction in the levels of these antioxidants [62, 67]. Previous study has shown that the micronutrient status of a pregnant woman is an important determinant of foetal growth and survival, [68] and multiple micronutrient deficiencies during pregnancies are said to be common in developing countries, [69] including Nigeria. Since poor nutrition and micronutrients deficiencies are known to aggravate malaria anaemia and other impacts of malaria on pregnancy, [71, 72] there is absolute need to streamline the nutritional requirements of our pregnant women in order to guide our pregnancy care-givers accurately on the use of supplements. Thus, it has been advocated that more attention be directed to the improvement of the nutritional status of our rural populace to improve the health and immune status of the pregnant women therein [73]. Therefore, studies geared towards understanding the effects of normal pregnancy on antioxidant micronutrients, and their correlation with one another during parturition are of paramount importance in this environment. As at now, even pre-pregnancy care, an aspect of obstetrics practice, has not received the needed attention [74]. Likewise, basal levels of oxidant and antioxidant parameters in normal pregnancy, that should form the guidelines for the choice of supplements, have not been well elucidated. This calls for concerted efforts by our scientists to take in-depth look at the pre-pregnancy conditions of our women, and factors that may affect pregnancy outcomes in apparently normal parturition, including general nutrition and specifically, antioxidant micronutrients. The later will form the basic values for comparison in cases of pregnancy complications where diagnoses are usually urgently needed. It will not only help our pregnancy care-givers in their choices of supplements but be a guide on dietary advice during pregnancy. Presently, most of the documented studies from our environment, [15, 23, 24, 70, 75] which also involved few antioxidants in each case, were from urban areas, with the exception of one [62]. Therefore, there is an overriding need to establish the reference values of these parameters in normal pregnancy within each locality. This will help to draw a good conclusion on the influence of oxidative stress on pregnancy outcomes, and also help to detect when a particular pregnancy is in danger due to oxidative stress. By this, we would have taken a right step to solving most feto-maternal problems for the attainment of Millennium Development Goals MDGs. References [1] Cotovio J, Onno L, Justine P, Lamure S, Catroux P. Generation of oxidative stress in human cutaneous models following in vitro ozone exposure. Chemosphere ; 67 1 Domain formation and orbital ordering transition in a dropped Jahn — Teller insulator. Phys Rev Lett ;97 17 Macrophage oxidative burst and related cytotoxicity. Differential activation by tumor-promoting and non-tumor-promoting phorbol esters. 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Endothelial nitric oxide synthase gene polymorphism in women with idiopathic recurrent miscarriage. Su MT, Lin SH, Chen YC. Genetic association studies of angiogenesis-and vasoconstriction-related genes in women with recurrent pregnancy loss: a systematic review and meta-analysis. Hum Reprod Update. Download references. Department of Obstetrics and Gynecology, University Clinical Center of Kosovo, , Prishtina, Kosovo. Department of Abdominal Surgery, University Clinical Center of Kosovo, , Prishtina, Kosovo. You can also search for this author in PubMed Google Scholar. VjAZ performed literature searches and wrote the manuscript. VaAZ and EK revised the manuscript. All authors read and approved the final manuscript. Correspondence to Vjosa A. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4. 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Review Open access Published: 16 October The role of oxidative stress in patients with recurrent pregnancy loss: a review Vjosa A. Zejnullahu ORCID: orcid. Methods We conducted literature search of published studies in the English language focusing on oxidative stress and its association with recurrent pregnancy loss RPL utilizing the Medline and Cochrane databases from through January Results The search yielded publications, of which 92 were included in the final analysis. Conclusions Future research in this field can provide new insights regarding the OS-mediated damage in recurrent pregnancy loss as well as potential applications of antioxidant therapy in this group of patients. Background By definition a pregnancy loss includes all pregnancy losses from the time of conception until 24 weeks of gestation or before the fetus reaches viability. Methods This article is a narrative overview of some original studies and review papers regarding the role of oxidative stress in pregnancy outcome, particularly focusing on oxidative stress and its association with recurrent pregnancy loss RPL. Study selection Literature related to the focused purpose of the study and studies published during the outlined time frame were included. Data extraction Data extraction was performed from the abstracts and full text and consisted of following information authors, publication year, research questions, study design and objectives, study outcome and recommendations. Results Search flow From the original search reviewers identified records through database searching of which were excluded with reason, did not match with the study criteria, duplicates, other manuscript types, irrelevant to topic. Flow diagram of narrative review of literature. Full size image. Main text By-products of O 2 metabolism, detoxification mechanisms and the role of oxidative stress Mitochondrial oxidative phosphorylation is the final stage of cellular respiration, following glycolysis, pyruvate oxidation and the citric acid cycle. Oxidative stress OS and oxidative biomarkers in recurrent pregnancy loss RPL Oxidative biomarkers are important tool in measuring oxidative stress in clinical samples in different pathologies. Antioxidant defense mechanisms and recurrent pregnancy loss RPL Because generation of reactive oxygen species ROS is the result of the aerobic cellular respiration and ATP production, living systems have developed necessary defense mechanisms against oxygen toxicity to maintain a delicate homeostatic balance between oxidant and antioxidant state. Angiogenesis and apoptosis-related genes and recurrent pregnancy loss RPL Another emerging field of investigations in the etiology of RPL include angiogenesis and apoptosis-related genes. Nitrosative stress NS and recurrent pregnancy loss The increased body of evidence associates nitrosative stress with recurrent pregnancy loss RPL. Conclusions This integrative overview based on the results of previous studies has shown that oxidative and nitrosative stress play an important role in the etiopathogenesis of early pregnancy loss and recurrent pregnancy loss. Availability of data and materials Medline and Cochrane databases. References ESHRE Guideline Group on RPL, Bender Atik R, Christiansen OB, Elson J, Kolte AM, Lewis S, Middeldorp S, et al. Article Google Scholar Andersen AM, Wohlfahrt J, Christens P, Olsen J, Melbye M. Article PubMed Central Google Scholar Lucas ES, Dyer NP, Murakami K, Hou Lee Y, Chan YW, Grimaldi G, et al. Article PubMed CAS Google Scholar Glueck CJ, Wang P, Goldenberg N, Sieve-Smith L. Article PubMed CAS Google Scholar Zidi-Jrah I, Hajlaoui A, Mougou-Zerelli S, Kammoun M, Meniaoui I, Sallem A, et al. 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Women having a history of vitamin supplementation before pregnancy, having prolonged hypertension either essential or next to renal disease, endocrine disease, anemia, malnutrition, mal-absorption, or other diseases , multiple pregnancies and abnormal levels of serum creatinine i. The Institutional Review Panel sanctioned the study procedure. Pre-eclampsia remained categorized mild least one or more of the subsequent signs or indications were existing wherein situation the pre-eclampsia was ordered as severe 8. Out of patients, 90 patients did not follow up until the end of the study period due to unexplained reasons. Fasting venous blood testers were collected in heparin-coated tubes. Plasma was parted by centrifugation and initially kept at ºC to be analyzed later but within one week. The α-tocopherol level was tested using means of HPLC high-pressure liquid chromatography. High-performance liquid chromatography is a technique in analytical chemistry used to separate, identify, and quantify each component in a mixture. It relies on pumps to pass a pressurized liquid solvent containing the sample mixture through a column filled with a solid adsorbent material causing different flow rates for the different components and leading to the separation of the components as they flow out of the column. A and B-carotene and vitamin C were analyzed by Micro techniques of clinical chemistry by Samuel Natelson Platelet count was done by fractional centrifugation after citric acid blood coagulation 9, A hour urine sample was collected for proteinuria estimation by the urine dipstick method. Statistical software SPSS version 21 was used for data feeding and analysis. A descriptive statistical analysis of continuous variables was performed. Data on continuous variables i. All the parameters were statistically evaluated by the Chi-square test after the study period. The mean maternal age of the severe cases of pregnancy-induced hypertensive was mean±SD The mean weight of normal pregnant women was Table 1: Clinical parameters of normal pregnant and pregnancy induced hypertensive women. There was no increase in the mean weight of pregnancy-induced hypertension PIH cases compared to the control, because of their comparative lower gestational ages, which were mean±SD The mean gestational age of the controls was The mean height of all respective groups was non-significant. The mean birth weight of mild cases was 2. The increase in systolic Proteinuria was detected in 3 7. Serum alpha-tocopherol vitamin E Table 2 was significantly low in severe and mild cases 0. Table 2: Comparison of the antioxidant nutrient profile among normal pregnant and pregnancy induced hypertensive women. Showed Alpha-tocopherol or vitamin E 0. Table 2 and Figure 1 compare the antioxidant nutrient profile among the three groups A, B and C, respectively. In terms of percentage presence of vitamin C in serum was This percentage of vitamin C was reduced as Further serum reduction of vitamin C as Results of vitamin E a-tocopherol levels in the serum were observed as The percentage of serum intensities of vitamin E was decreased to In contrast, the serum levels of vitamin E remained further decreased to Results were observed as B-carotene levels in the serum were The percentage serum levels of 0-carotene were reduced to Results were observed as vitamin A levels in the serum as The percentage of serum levels of vitamin A was reduced slightly to The serum levels of vitamin A remained the same as Figure 1: Comparison of the antioxidant nutrient profile among normal pregnant and pregnancy induced hypertensive women. The main contributor to maternal and fetal death and morbidity is preeclampsia. Oxidative stress has been associated with the pathophysiology of preeclampsia. Falling by the levels of the antioxidant nutrients observed in this study indirectly proposes an idea that hyperexcitation of free radicals mediated lipid peroxidation and the comparative utilization of antioxidants may be involved in the pathophysiological mechanism pregnancy-induced hypertension Physiologic irregularities of preeclampsia have been attributed to abnormalities in endothelial cells of maternal vessels due to the emergence of free radicals from the defective placenta The main oxidation product of α-tocopherol is a tocopherylguinone, which can be conjugated to give glucuronate after the previous lessening with hydroquinone. It is expelled in the bile or additional degraded in the kidneys to α- tocopheryl acid and thus emitted in the bile. Vitamin E proteins not selected preferentially by the hepatic binding proteins are removed during the secretory process of very-low-density lipoprotein VLDL in the liver and probably excreted by the bile. Part of vitamin E can also be excreted by cutaneous sebaceous glands The role of nourishment in usual and unusual gestations has long been discussed. Our results determine that plasma levels of ascorbic acid were expressively reduced in mild and severe patients of pregnancy-induced hypertension, while alpha-tocopherol and beta-carotene levels were meaningfully reduced only in patients with severe cases of pregnancy-induced hypertension. These discoveries are comparable to those distinguished by Al-Gubory Our study showed decrease in vitamin A concentrations in mild and severe cases stayed insignificant despite its substantial singlet oxygen scavenging ability. The possible share of vitamin A and other retinoids in malignancy prevention has however been reviewed recently In patients with pregnancy-induced hypertension, we hypothesize that antioxidant nutrients may be used to gain further free radical-induced cells endometrial movement, resulting in a decrease in antioxidant levels. Water-soluble nutrient, the ascorbic acid lipid-soluble antioxidant is seen initially and then followed antioxidants, Tocopherol alpha, and beta-carotene. Several findings are worth mentioning. Initially, smoking is known to reduce plasma antioxidant nutrient concentrations, mostly those of ascorbic acid and beta-carotene in this study, there were no smokers. An antioxidant nutrient level in smaller studies indicates that the independent effects of smoking The concentration of the antioxidant nutrients can be predisposed thru several reasons, as well as nutritional intake. In this study, we cannot complete a nutritive assessment. Some examples may be a solemn assembly to deny that they are all fears of the recent fast blow of nutrient intake because of the chastisement of a union. If it is excluded from the study of patients with abnormally high levels of creatinine, renal function may be the removal of nutrients. People now repeatedly take multivitamin supplements too during pregnancy and women who are excluded, since supplements can be produced to support any issues. In short, the very homogeneous with what they were once equally subject to socioeconomic image of the same region, has recruited a sufficient catchment customer. The mean maternal age and parity of the severe cases of pregnancy-induced hypertension were significantly low compared to normal pregnancy. Primigravida and teenagers were at a higher risk of developing the disease. There is a sharp rise in incidence above the age of 35 years 18, The main purpose of selecting control cases with a lower parity was to avoid malnutrition and anemia in such women, which is commonly seen in women with high parity and poor socioeconomic conditions. The present outcomes remain in settlement through a current finding of decreased antioxidant action in females having pregnancy-induced hypertension. In normal gestation, there is an alteration in the percentage of vitamin E to lipid peroxides in maternal blood that gradually favors vitamin E through progressing pregnancy Sarwar et al. in their study also proved that vitamin E levels were unchanged in mild cases of pregnancy-induced hypertension but were significantly decreased in severe cases The proportion of lipid peroxides to alpha tocopherol was improved in mild. Besides, it significantly improved in severe cases of pregnancy-induced hypertension. Alpha tocopherol is a free radical scavenger and thus applies antioxidant action. On the other hand, alpha-tocopherol is used in applying its usage, so unusual upsurges in lipid peroxides in pregnancy-induced hypertension would increase consumption, resulting in the increased alpha-tocopherol levels Concentrated ascorbic acid is a bio-available type of ascorbic acid. This works as per the antioxidant is transformed from the reduced to the oxidized pattern. It has been reported that ascorbic acid is a hydrophilic antioxidant act as a first-line antioxidant against oxygen particles, which appear mainly in plasma. Unlikely, alpha-tocopherol and beta-carotene are the hydrophobic antioxidants that can quench oxygen free radicals, which are mainly present in the membrane of lipid cells Ascorbic acid and free radicals that entraps a major part of the water is present in the plasma. Since ascorbic acid exceeded the capability of free radicals in the cell membrane through extensive lipid peroxidation, which can be inhibited by the disclosure of alpha-tocopherol and beta-carotene Co-antioxidants i. The right levels of vitamin C maintain and strengthen the powerful antioxidant, namely vitamin E. Decreasing the levels of the antioxidant nutrients witnessed in this study indirectly sustenance an idea that hyper excitation of free radicals mediated lipid peroxidation and the relative utilization of antioxidants may be involved in the pathophysiological mechanism pregnancy-induced hypertension Our findings which were decreased in vitamin C levels in patients with mild and extreme hypertension caused by pregnancy; however, alpha-tocopherol and beta carotene concentrations merely decreased while the disease existed severe suggested that radical antioxidant interactions in pregnancy-induced hypertension might be introduced in the water-soluble part of the plasma. We estimate that the progress can then be transmitted as disease developments to the endothelial cell membrane. Serum alpha-tocopherol vitamin E was significantly low in severe and mild cases when compared with normal pregnant women levels 0. An improved understanding of pregnancy-induced hypertension and its management is the main outcome of the study with good control PIH and safe prolongation of pregnancy until term. In Pakistan, severe preeclampsia due to pregnancy-induced hypertension is very common owing to low socioeconomic status and lack of prenatal care. The authors would like to acknowledge the staff of Jinnah Postgraduate Medical Centre for their support in data gathering. KA presented the idea and reviewed the manuscript; AA did the literature review and FA contributed in critical review and statistical analysis. AJ assisted in research write up, NA helped in analysis and editing and SR performed the review of manuscript. This is an open-access article distributed under the terms of the CreativeCommons Attribution License CC BY 4. DOWNLOAD PDF. Department of Physiology, Jinnah Sindh Medical University. Department of Biochemistry, Jinnah Sindh Medical University, Karachi, Pakistan. ABSTRACT Background: Preeclampsia is a multifactorial disorder leading to complications of pregnancy. |
Free radicals and pregnancy complications -
This entry is adapted from the peer-reviewed paper oxidative stress pregnancy preeclampsia antioxidants. Oxidative Stress in Normal Pregnancies As the placenta develops, it transits from a hypoxic environment to a more oxygenated setting.
The period of placental development is characterised by a low grade of OS, increased circulating levels of oxidised low-density lipoproteins LDL , and a reduction in total antioxidant capacity TAC. A recent study by Mannaerts et al. ROS are necessary for certain cellular functions, such as mitochondrial or endothelial functions, normally in low and stable levels.
Redox signalling is pivotal in many physiological processes, whereby oxidative post-translational modifications induce changes in structural and functional characteristics of molecules, thus modifying signalling processes [ 2 ].
However, elevated levels of ROS, as observed in pathologic pregnancies, are associated with adverse outcomes, including tissue and mitochondrial damage and accelerated aging. During the first 6—8 weeks of pregnancy, with the placenta not yet completely attached to maternal circulation, the uterine spiral arteries are blocked by intraluminal cytotrophoblast and a physiological and local hypoxia is generated.
In this period, since the syncytiotrophoblast cells do not express the antioxidant mitochondrial superoxide dismutase SOD , ROS levels are high, inducing the production of factors that regulate cell proliferation and angiogenesis, such as vascular endothelial growth factor VEGF and placental growth factor PlGF , which are abundantly expressed in the placenta [ 3 ].
The angiogenic signalling pathway is tightly regulated at various levels, such as a soluble Fms-like tyrosine kinase-1 sFlt-1 , acting as a decoy receptor to neutralize the pro-angiogenic effects from VEGF and PIGF.
Maternal blood levels of sFlt-1 and PlGF have been analysed extensively [ 4 ] and are utilised as key biomarkers during pregnancy see below. Unblocking of the spiral arteries begins at 8 weeks and continues until 16 weeks of gestation. While spiral arteries lose their muscular layer and transform into a large vessel with low resistance, an increased oxygen tension is quickly imposed, bringing the associated risks of damage from OS.
In non-pathological concentrations, OS stimulates cell proliferation. However, with premature opening unplugging of the spiral arteries, the placental growth is prejudiced since there is insufficient antioxidant defence by this time.
A deficiency in the early development of the placenta restricts its growth, which can never be catch up [ 5 ]. From a chemical point of view, these periods of ischemia followed by reperfusion are associated with the conversion of xanthine dehydrogenase into xanthine oxidase, which is a potent source of superoxide free radicals, thus increasing OS.
It has been demonstrated that xanthine oxidase activity is increased in the placenta of women affected by HDP. In addition, a lower production of NO is related to the peripheral vasoconstriction observed in preeclampsia [ 6 ].
The third trimester is the period of maximum growth of both the placenta and the foetus, corresponding to a great increase in placental vascular and energetic requests. During this stage, the highly metabolic placenta relies on efficient mitochondrial function to produce the necessary energy.
In this scenario, a hypovolemic state could progress to placental hypoperfusion and, therefore, to foetal growth restriction. During pregnancy, the maternal cardiovascular system adapts to the increased demand, resulting in an increase in cardiac output, stroke volume, heart rate, and plasma volume.
The heart undergoes significant remodelling to keep up with the demand. Despite all these modifications, in most cases, maternal blood pressure remains stable, compensated by generalized peripheral vasodilation.
This vascular change is largely driven by a higher production of NO in endothelial cells [ 8 ]. NO is a prime target for inactivation by superoxide and this free radical is increased in preeclamptic pregnancies, thus explaining the generalized peripheral vasoconstriction observed in this pathological state.
This systemic vasoconstriction can be clinically observed in preeclampsia and acts as a major indicator of pregnancy complications. In the first trimester, uterine artery Doppler can be performed to assess the risk of preeclampsia. The uterine artery pulsatility index PI , defined as the difference between peak systolic and end diastolic flow velocity, divided by the time-averaged flow velocity [ 9 ] , provides a measure of uteroplacental perfusion.
A high PI index suggests an increased risk of developing PE, FGR, and stillbirth. Examples of normal and abnormal uterine artery doppler waveform in the first trimester are shown in Figure 1.
Moreover, maternal renal vasoconstriction favours hypertension and a modest reduction in glomerular filtration rate with a latter disruption of glomerular fenestrae, causing proteinuria.
Figure 1. Abnormal top and normal bottom uterine artery Doppler waveform in the first trimester. While systolic velocities are similar, the lower waveform show a low resistance vessel with broader systolic peak, as well as a continuous diastolic flow, secondary to a complete remodelling of the spiral arteries.
Although the main focus of this entry is OS damage in pregnancy concerning the foetus and the mother, it is important to note that OS influences the entire reproductive lifespan of women and men.
There has been a considerable amount of work regarding oxidative damage in sperm and oocytes. Male gametes are sensitive cells to the accumulation of damaged DNA, which can be induced by a wide variety of factors, such as diet [ 10 ] , ionization, or even heavy metals [ 11 ] [ 12 ].
Since DNA damage in the gametes could have serious consequences in reproduction [ 13 ] , the sperm may also play a role in complicated pregnancies.
Preeclampsia is a disease in which the mother develops high blood pressure after 20 weeks of pregnancy and presents with proteins in her urine, alterations in blood test, or clinical symptoms such as severe headache, abdominal pain, or visual alterations.
The only cure available for this clinical entity is delivery, which can represent a major disadvantage for the foetus if the pregnancy is not advanced, adding prematurity to a possible suboptimal development.
During the first trimester, abnormal and asymptomatic placentation occurs, followed by a symptomatic maternal syndrome that carries an excess of antiangiogenic factors. See Figure 2 for an overview of the main events in the development of preeclampsia.
Figure 2. Main events in the development of preeclampsia. According to the timing of clinical onset, before or after 34 weeks of gestation, preeclampsia is classified as early-onset preeclampsia EoPE and late-onset preeclampsia LoPE , respectively. Although foetuses at this point are already more developed, they are at risk of being either small or large for gestational age and they tend to have less adaptability and can rapidly deteriorate [ 18 ].
Despite the classification of EoPE and LoPE attributing the cause to the placenta and maternal, respectively, it is important to clarify that the combination of both maternal and placental factors can contribute to the development of both types of preeclampsia.
OS provides one explanation for the pathogenesis of preeclampsia since it leads to lipid peroxidation accompanied by endothelial dysfunction, i. A vicious cycle of enhanced placental OS can allow the release of leukocytes, neutrophils, and cytokines from the placenta, as well as further ROS into the maternal blood circulation, resulting in a massive systemic endothelial dysfunction.
In cases where great endothelial damage is observed, arterial compliance is lower and vascular resistance is higher [ 19 ].
Furthermore, as widely demonstrated in the Framingham Heart Study [ 20 ] , arterial stiffness acts as a predictor of cardiovascular disease, cognitive impairment, and dementia. Elevated ROS levels could also provide the cause for early elevation of antiangiogenic or decrease in angiogenic factors at a time when the placenta needs more vascular development.
There is abundant evidence of higher serum and tissue concentrations of biomarkers for OS and systemic inflammation, as well as decreased concentrations of antioxidants, such as vitamin C and vitamin E in women with preeclampsia [ 21 ].
However, a major challenge in recent decades has been to establish reliable biomarkers for the early detection and prediction of pregnancy complications.
Identifying a circulatory biomarker can have major clinical impacts, especially if they can provide early opportunities for clinical intervention. Unfortunately, to date, both predictive and diagnostic biomarkers have rarely been successful. Several molecules related to OS stress have been proposed, since there are direct chemical interactions between ROS and biological components in preeclampsia.
Nevertheless, most of these biomarkers are diagnostic, meaning they are elevated by the time the disease is clinically present, thus with scarce predictive capacity. Glutathione GSH , one of the most prevalent antioxidants, can reduce unstable ROS and form oxidized GSH.
Reduced GSH represents the most prevalent form of GSH in the organism and the ratio of reduced GSH and oxidized GSH can be used to demonstrate levels of OS.
In a study conducted by Kharb et al. With regards to the lower levels of reduced GSH seen in preeclamptic patients, it is important to note that an association between the use of paracetamol acetaminophen and the depletion of GSH has been described [ 23 ].
Paracetamol is one of the most consumed drugs during pregnancy, not limited to hypertensive women. Although it is feasible to speculate that paracetamol may be responsible for lower GSH levels, it is doubtful that such a chronic effect would be sustained. Further investigations are needed in order to elucidate the eventual correlation between this worldwide used drug and the antioxidant capacity during pregnancy.
In response to OS, protein carbonyls are generated and researchers have shown elevated levels of these molecules in plasma [ 25 ] and placentas [ 26 ] [ 27 ] of preeclamptic women during the clinical stage.
However, higher levels of protein carbonyls were also described in pregnancies complicated with GDM [ 28 ] , making these molecules a poorly specific biomarker.
FGR or intra-uterine growth restriction IUGR is a common pregnancy pathology in which the foetus is unable to achieve its genetically determined potential size and weight. They carry a higher risk of long-term complications, such as poor cognitive performance, growth retardation, as well as lifelong risk of cardiovascular disease and metabolic syndrome.
Since the main cause is placental dysfunction, it has been associated with elevated OS. Placentas from pregnancies with FGR have a significantly decreased expression of genes involved in mitochondrial function and oxidative phosphorylation but higher markers of OS [ 30 ]. Additionally, elevated levels of oxidized low-density lipoproteins Ox-LDL in placental tissue have been shown in patients with preeclampsia and FGR.
A major issue with utilising oxidative stress biomarkers for pregnancy complications is that labour activates oxidative stress in the placenta [ 31 ] , which can lead to wrong conclusions. Care needs to be taken when interpreting results from placenta and blood taken post-delivery.
Studies that have monitored blood levels of ROS during pregnancies with FGR have shown an increased level of MDA—a breakdown product of lipid peroxidation [ 32 ] , as well as reduced plasma TAC [ 33 ] both in maternal plasma, placental tissue [ 34 ] , and cord blood in the infants [ 35 ].
Pregnancy-associated plasma protein-A PAPP-A is a protein also related to FGR. It is synthesized by the decidua and measurable in maternal blood in early pregnancy.
One of its functions is to cleave IGFBP-4, an insulin growth factor IGF inhibitor, thus augmenting the activity of IGFs. Lower levels of PAPP-A are associated with an increased risk for FGR.
GDM is usually a transient hyperglycaemic state brought on by pregnancy and linked to insulin dysregulation. However, GDM and type 2 diabetes share a common pathogenesis related to insulin resistance or β-cell dysfunction.
It represents an important gestational disorder and a precursor for lifetime disease, since up to half of women with a history of GDM will develop type 2 diabetes five to ten years after delivery [ 37 ]. Following NICE Guidelines [ 38 ] , pregnant patients are offered a 75 g 2 h oral glucose tolerance test OGTT at 24 to 28 weeks.
In the last three decades, prevalence of GDM has increased ostensibly in all countries despite the income levels WHO, As in preeclampsia, increased ROS and lower plasma antioxidant capacity occur in association with an altered maternal metabolic environment, and GDM is frequently associated with systemic and chronic inflammation.
It has been observed that insulin resistance reduces mitochondrial respiration [ 39 ] and that human umbilical cord mesenchymal stromal cells from patients with GDM have premature senescence phenotypes and mitochondrial dysfunction. Elevated levels of AGEs are also observed in patients with preeclampsia [ 41 ].
Moreover, hyperglycaemia has been found to upregulate NADPH oxidase, whose primary role is to generate ROS [ 42 ]. As shown by Leloup et al. Furthermore, insulin secretion can be induced by mitochondrial ROS. It has been demonstrated that incubation of trophoblast from normal placentas, with glucose at a concentration similar to in vivo hyperglycaemic levels, also generates a rise in MDA [ 30 ].
Other molecules involved in OS and GDM are F2-isoprostanes, formed mostly by the peroxidation of arachidonic acid. They have an important role in organ vasoconstriction, including in the kidney and the placenta, and can be detected in the plasma and urine of diabetic and preeclamptic pregnant women.
Kapustin et al. OS plays an important role, not only in preeclampsia and GDM, but in several disorders which represent risk factors for complicated pregnancy and subsequent and possible pre- comorbidities, i.
Vascular endothelium consists of a single but complex layer of epithelial cells covering the interior surface of blood vessels. This organ is responsible for controlling the passage of molecules in and out of the bloodstream; has paracrine and autocrine functions; and plays a role in inflammatory cell adherence, anticoagulation, and angiogenesis.
Endothelial dysfunction is a key event in the development of vascular diseases and it is enhanced by OS, leading to cardiac failure, peripheral artery disease, diabetes mellitus, and stroke [ 30 ].
It is a state characterized by vasoconstriction, inflammation, and prothrombotic tendency. On a chemical pathway, excessive production of ROS induces oxidation of tetrahydrobiopterin BH4 , a cofactor of endothelial NOS, which produces NO from l-arginine.
PLoS One. Sudharshana Murthy KA, Bhandiwada A, Chandan SL, Gowda SL, Sindhusree G. Evaluation of Oxidative Stress and Proinflammatory Cytokines in Gestational Diabetes Mellitus and Their Correlation with Pregnancy Outcome.
Indian J Endocrinol Metab. Obeagu EI, Bunu UO, Obeagu GU, Habimana JB. Antioxidants in the management of sickle cell anaemia: an area to be exploited for the wellbeing of the patients.
Obeagu EI, Ubosi NI, Uzoma G. Antioxidant Supplementation in Pregnancy: Effects on Maternal and Infant Health. Int J Adv Multidiscip Res. Utilization of Antioxidants in the management of diabetes mellitus patients.
J Diabetes Clin Prac. Nwosu DC, Obeagu EI, Nkwocha BC, Nwanna CA, Nwanjo HU, Amadike JN, Elendu HN, Ofoedeme CN, Ozims SJ, Nwankpa P. J Bio Innov ; 5 1 Obeagu EI, Obeagu GU, Obiezu J, Ezeonwumelu C, Alum EU, Ugwu OP. Antioxidants and Pregnancy: Impact on Maternal and Fetal Health.
APPLIED SCIENCES NIJBAS. Ilekis JV, Tsilou E, Fisher S, Abrahams VM, Soares MJ, Cross JC, Zamudio S, Illsley NP, Myatt L, Colvis C, Costantine MM, Haas DM, Sadovsky Y, Weiner C, Rytting E, Bidwell G. Placental origins of adverse pregnancy outcomes: potential molecular targets: an Executive Workshop Summary of the Eunice Kennedy Shriver National Institute of Child Health and Human Development.
Am J Obstet Gynecol. Epub Mar Diniz MS, Magalhães CC, Tocantins C, Grilo LF, Teixeira J, Pereira SP. Nurturing through Nutrition: Exploring the Role of Antioxidants in Maternal Diet during Pregnancy to Mitigate Developmental Programming of Chronic Diseases.
Hussain T, Tan B, Liu G, Murtaza G, Rahu N, Saleem M, Yin Y. Modulatory Mechanism of Polyphenols and Nrf2 Signaling Pathway in LPS Challenged Pregnancy Disorders. Epub Aug Agarwal A, Aponte-Mellado A, Premkumar BJ, Shaman A, Gupta S.
The effects of oxidative stress on female reproduction: a review. Reprod Biol Endocrinol. Xu K, Liu G, Fu C. The Tryptophan Pathway Targeting Antioxidant Capacity in the Placenta. Nwakuilite A, Nwanjo HU, Nwosu DC, Obeagu EI.
Evaluation of enzyme antioxidants in streptozocin-induced diabetic rats treated with Moringa oleifera leaf powder. European Journal of Biomedical. Ifeanyi OE. A review on free radicals and antioxidants. Akinpelu M, Gamade SM, Akinbo F, Adeniyi TD, Elizebeth AF, Obeagu EI.
Histopathological and Biochemical Effect of Vitamin C and D on Phosphine-Induced Hepatotoxicity in Wistar Rats. Asian Journal of Dental and Health Sciences. Nwakulite A, Obeagu EI, Eze R, Ugochi VE, Vincent CC, Okafor CJ, Chukwurah EF, Unaeze BC, Amaechi CO, Okwuanaso CB, Chukwuani U. Estimation of Serum Glutathione Peroxidase in Streptozotocin-Induced Diabetic Rat Treated with Bitter Leaf Extract.
Journal of Pharmaceutical Research International. Ifeanyi OE, Stella EI, Favour AA. Antioxidants in the Management of Sickle Cell Anaemia.
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The Role of Oxidative Stress and Antioxidant Balance in Pregnancy. Mediators Inflamm. Chiarello DI, Abad C, Rojas D, Toledo F, Vázquez CM, Mate A, Sobrevia L, Marín R. Oxidative stress: Normal pregnancy versus preeclampsia. Biochim Biophys Acta Mol Basis Dis. Epub Dec Tenório MB, Ferreira RC, Moura FA, Bueno NB, de Oliveira ACM, Goulart MOF.
Cross-Talk between Oxidative Stress and Inflammation in Preeclampsia. Guerby P, Tasta O, Swiader A, Pont F, Bujold E, Parant O, Vayssiere C, Salvayre R, Negre-Salvayre A. Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia. Redox Biol.
Epub Jan Anyiam AF, Obeagu EI, Obi E, Omosigho PO, Irondi EA, Arinze-Anyiam OC, Asiyah MK. ABO blood groups and gestational diabetes among pregnant women attending University of Ilorin Teaching Hospital, Kwara State, Nigeria.
International Journal of Research and Reports in Hematology. Obeagu EI. Gestational Thrombocytopaenia. Sánchez-Aranguren LC, Prada CE, Riaño-Medina CE, Lopez M. Endothelial dysfunction and preeclampsia: role of oxidative stress. Front Physiol. Obeagu EI, Ogbonna US, Nwachukwu AC, Ochiabuto O, Enweani IB, Ezeoru VC.
Prevalence of Malaria with Anaemia and HIV status in women of reproductive age in Onitsha, Nigeria. Gerber PA, Rutter GA. The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus. Antioxid Redox Signal. Epub Jun Obeagu EI, Abdirahman BF, Bunu UO, Obeagu GU.
Obsterics characteristics that affect the newborn outcomes. Int J Adv Res Biol Sci. Oxidative stress, placental ageing-related pathologies and adverse pregnancy outcomes.
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Iron Status of Pregnant and Post-Partum Women with Malaria Parasitaemia in Aba Abia State, Nigeria. Annals of Clinical and Laboratory Research. Eze RI, Obeagu EI, Edet FN.
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Assessment of some haematological parameters in malaria-infected pregnant women in Imo state Nigeria. Int J Curr Res Biol Med. Review: Placental mitochondrial function and structure in gestational disorders.
Lu M, Sferruzzi-Perri AN. Placental mitochondrial function in response to gestational exposures. Epub Dec 5. Obeagu EI, Njar VE, Obeagu GU. Infertility: Prevalence and Consequences. Emeka-Obi OR, Ibeh NC, Obeagu EI, Okorie HM. Evaluation of levels of some inflammatory cytokines in preeclamptic women in Owerri.
Obeagu EI, Faduma MH, Uzoma G. Ectopic Pregnancy: A Review. The roles of Neutrophils in pregnancy. In patients with pregnancy-induced hypertension, we hypothesize that antioxidant nutrients may be used to gain further free radical-induced cells endometrial movement, resulting in a decrease in antioxidant levels.
Water-soluble nutrient, the ascorbic acid lipid-soluble antioxidant is seen initially and then followed antioxidants, Tocopherol alpha, and beta-carotene.
Several findings are worth mentioning. Initially, smoking is known to reduce plasma antioxidant nutrient concentrations, mostly those of ascorbic acid and beta-carotene in this study, there were no smokers.
An antioxidant nutrient level in smaller studies indicates that the independent effects of smoking The concentration of the antioxidant nutrients can be predisposed thru several reasons, as well as nutritional intake.
In this study, we cannot complete a nutritive assessment. Some examples may be a solemn assembly to deny that they are all fears of the recent fast blow of nutrient intake because of the chastisement of a union. If it is excluded from the study of patients with abnormally high levels of creatinine, renal function may be the removal of nutrients.
People now repeatedly take multivitamin supplements too during pregnancy and women who are excluded, since supplements can be produced to support any issues.
In short, the very homogeneous with what they were once equally subject to socioeconomic image of the same region, has recruited a sufficient catchment customer. The mean maternal age and parity of the severe cases of pregnancy-induced hypertension were significantly low compared to normal pregnancy.
Primigravida and teenagers were at a higher risk of developing the disease. There is a sharp rise in incidence above the age of 35 years 18, The main purpose of selecting control cases with a lower parity was to avoid malnutrition and anemia in such women, which is commonly seen in women with high parity and poor socioeconomic conditions.
The present outcomes remain in settlement through a current finding of decreased antioxidant action in females having pregnancy-induced hypertension.
In normal gestation, there is an alteration in the percentage of vitamin E to lipid peroxides in maternal blood that gradually favors vitamin E through progressing pregnancy Sarwar et al. in their study also proved that vitamin E levels were unchanged in mild cases of pregnancy-induced hypertension but were significantly decreased in severe cases The proportion of lipid peroxides to alpha tocopherol was improved in mild.
Besides, it significantly improved in severe cases of pregnancy-induced hypertension. Alpha tocopherol is a free radical scavenger and thus applies antioxidant action.
On the other hand, alpha-tocopherol is used in applying its usage, so unusual upsurges in lipid peroxides in pregnancy-induced hypertension would increase consumption, resulting in the increased alpha-tocopherol levels Concentrated ascorbic acid is a bio-available type of ascorbic acid.
This works as per the antioxidant is transformed from the reduced to the oxidized pattern. It has been reported that ascorbic acid is a hydrophilic antioxidant act as a first-line antioxidant against oxygen particles, which appear mainly in plasma.
Unlikely, alpha-tocopherol and beta-carotene are the hydrophobic antioxidants that can quench oxygen free radicals, which are mainly present in the membrane of lipid cells Ascorbic acid and free radicals that entraps a major part of the water is present in the plasma.
Since ascorbic acid exceeded the capability of free radicals in the cell membrane through extensive lipid peroxidation, which can be inhibited by the disclosure of alpha-tocopherol and beta-carotene Co-antioxidants i. The right levels of vitamin C maintain and strengthen the powerful antioxidant, namely vitamin E.
Decreasing the levels of the antioxidant nutrients witnessed in this study indirectly sustenance an idea that hyper excitation of free radicals mediated lipid peroxidation and the relative utilization of antioxidants may be involved in the pathophysiological mechanism pregnancy-induced hypertension Our findings which were decreased in vitamin C levels in patients with mild and extreme hypertension caused by pregnancy; however, alpha-tocopherol and beta carotene concentrations merely decreased while the disease existed severe suggested that radical antioxidant interactions in pregnancy-induced hypertension might be introduced in the water-soluble part of the plasma.
We estimate that the progress can then be transmitted as disease developments to the endothelial cell membrane. Serum alpha-tocopherol vitamin E was significantly low in severe and mild cases when compared with normal pregnant women levels 0. An improved understanding of pregnancy-induced hypertension and its management is the main outcome of the study with good control PIH and safe prolongation of pregnancy until term.
In Pakistan, severe preeclampsia due to pregnancy-induced hypertension is very common owing to low socioeconomic status and lack of prenatal care. The authors would like to acknowledge the staff of Jinnah Postgraduate Medical Centre for their support in data gathering.
KA presented the idea and reviewed the manuscript; AA did the literature review and FA contributed in critical review and statistical analysis. AJ assisted in research write up, NA helped in analysis and editing and SR performed the review of manuscript.
This is an open-access article distributed under the terms of the CreativeCommons Attribution License CC BY 4. DOWNLOAD PDF. Department of Physiology, Jinnah Sindh Medical University.
Department of Biochemistry, Jinnah Sindh Medical University, Karachi, Pakistan. ABSTRACT Background: Preeclampsia is a multifactorial disorder leading to complications of pregnancy.
The authors declare no conflict of interest. The written and verbal consents were obtained for the research. Katsiki N, Godosis D, Komaitis S, Hatzitolios A. Hypertension in pregnancy: classification, diagnosis and treatment. Aristotle Univ Med J. Chen Q, Sousa JD, Snowise S, Chamley L, Stone P.
Reduction in the severity of early onset severe preeclampsia during gestation may be associated with changes in endothelial cell activation: A pathological case report.
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Either your web browser doesn't support Javascript or it is currently complicatons off. In the Free radicals and pregnancy complications case, please turn on Radiclas support in your Organic browser Free radicals and pregnancy complications complicationns this page. Review Articles rdicals the Open Access Subset are available under a Creative Commons license. This means they are free to read, and that reuse is permitted under certain circumstances. There are six different Creative Commons licenses availablesee the copyright license for this article to understand what type of reuse is permitted. Free full text in Europe PMC. The pathophysiological mechanism underlying pregnancy complications such as congenital malformations, miscarriage, preeclampsia, or fetal growth restriction is not entirely known.Free radicals and pregnancy complications -
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International Journal of Advanced Multidisciplinary Research. Assessment of coagulation parameters in malaria-infected pregnant women in Imo state, Nigeria. The oxidative stress is a consequence of excessive ROS production, reduced antioxidant capacity and mitochondrial dysfunction [ 22 , 23 ].
When oxidative stress OS occurs, macromolecular homeostasis can be substantially affected because of lipid peroxidation, protein modifications and DNA oxidation by free radicals [ 23 , 24 , 25 ]. At physiological levels ROS modulate cell cycle and proliferation, activate angiogenesis, enable phagocytosis, activate antioxidant genes and pro-inflammatory cytokines [ 22 , 24 , 26 , 27 ].
Low, physiological levels of ROS are necessary for self-renew of stem cells while increased ROS levels activate proliferation, differentiation, senescence and apoptosis of stem cells in concentration-dependent manner [ 28 ].
Detrimental effects on living organisms arise when ROS, exceed basal levels needed for cell signaling and transduction [ 22 ].
Therefore, the beneficial effects of ROS are achievable within physiological levels and deviation from redox window as oxidative or reductive stresses [ 29 ] will be associated with different pathologies including neurodegenerative diseases [ 30 ] diabetes [ 31 ] cardiovascular disease and atherosclerosis [ 32 ] rheumatoid arthritis [ 33 ] respiratory disease [ 34 ] carcinogenesis [ 35 ] ageing [ 36 ] female reproductive disease, pregnancy complications and recurrent pregnancy loss [ 37 ].
Oxidative biomarkers are important tool in measuring oxidative stress in clinical samples in different pathologies. Early pregnancy is characterized by increased level of polymorphonuclear leukocyte count, which in turn contribute to the oxidative stress because of superoxide generation from these primed leucocytes [ 39 ].
In women with recurrent abortions increased generation of radical species from leukocytes was demonstrated via increased granulocyte spontaneous chemiluminescence when compared to the reference group [ 40 ]. NADPH-oxidase found in polymorphonuclear leukocytes, present a major source of superoxide generation in early and term pregnancy [ 41 , 42 ].
NADPH oxidases Nox are a family of isoenzymes found in neutrophils, vascular smooth muscle cells and placenta [ 43 , 44 ]. Placental isoform or human placental NADPH oxidase has different properties compared to neutrophils and macrophages [ 43 ]. Evidence suggest that NADPH oxidase is the main source of superoxide generation before 10 weeks of gestation when chorionic villi are exposed to relative hypoxia [ 41 , 45 ].
A study investigating NADPH oxidase activity and antioxidant capacity in placental tissues from early and term pregnancies showed corresponding increase of antioxidant capacity and Nox activity emphasizing the role of superoxide production in modulation of antioxidant defense in early pregnancy [ 42 ].
Altered balance between oxidants and antioxidants can trigger oxidative stress in human placenta and has important implications in the etiology of RPL.
Studies investigating oxidants, consistently reported increased levels in plasma and placental tissues of recurrent miscarriage patients. Superoxide anion radical SOA is the most widespread ROS and an imbalance in the homeostatic concentrations of superoxide anion and H 2 O 2 can lead to the production of hydroxyl ions.
Significance of this highly reactive free radical is that can cause severe cell injury by reacting with organic and non-organic molecules [ 16 ]. A recent study reported significant increase of SOA in plasma samples of RPL patients compared to the control samples Similar difference was observed for the placental tissue SOA between the two groups 5.
Another parameter of oxidative stress assayed in plasma and placental tissue is H 2 O 2. Two studies assessing this biomarker yielded similar results. Ghneim et al. Comparably, Al-Sheikh and coauthors found increased levels of this marker in placental tissues of recurrent miscarriage patients 3.
Importantly, increased levels of SOA and H 2 O 2 in both studies were associated with depletion of enzymatic antioxidants such as superoxide dismutase SOD catalase CAT , glutathione reductase GR and glutathione peroxidase GPx as well as decreased expression of all examined antioxidant genes GPx, GR, SOD and CAT [ 8 , 9 ].
The superoxide dismutase SOD is one of the main antioxidant enzymes and its activity is regarded as a first line of defense in preventing oxidative stress OS. A study conducted to examine SOD1 and SOD2 activities in samples of RPL patients and controls found interesting results.
SOD1 plasma activity was 5. Similar results were observed for SOD2 plasma activity in study and control group 4. In this study increased levels of SOA were associated with concurrent decrease of SOD1 and SOD2 activity in plasma and placental tissues of women with RPL [ 46 ].
Yiyenoglu et al. Therefore, oxidative stress associated with deficient antioxidant defense is regarded as one of the key factors in the etiopathogenesis of RPL. It should be emphasized that reactive oxygen species ROS and reactive nitrogen species RNS can act together to induce cellular injury.
Nitric oxide NO is nitrogen based-reactive species and as membrane permeable radical can react with superoxide to form peroxynitrite, an agent with oxidizing and nitrating properties [ 48 ]. Therefore, NO can mediate ROS-induced lipid peroxidation LPO.
In particular polyunsaturated fatty acids PUFA are less resistant to free-radical attack because of the abundance of double bonds in their structure [ 49 ].
Malondialdehyde MDA is toxic end-product of autoxidation of polyunsaturated fatty acids PUFA and important index of oxidative damages. As a result of lipid peroxidation several membrane functions are disturbed including membrane permeability, fluidity and enzyme activity [ 48 ].
Studies evaluating the level of oxidative stress by assessing malondialdehyde MDA as a product of lipid peroxidation, have found elevated plasma and placental levels of this marker in patients with recurrent pregnancy loss RPL.
Reported plasma MDA levels were 5. A case—control study investigating the MDA levels in RPL patients, healthy pregnant and non-pregnant women found a significant elevation of this marker in the study group. El-Far et al. The authors conclude that possible oxidative damage due to the increased generation of oxidative species and diminished antioxidative defense may be responsible for recurrent abortions [ 51 ].
Although, mechanism by which oxidative stress OS contribute to anticardiolipin antibodies aCL formation is not fully clarified, a study conducted by Ferro et al. Another study evaluating extent of somatic DNA damages and oxidative stress conditions found a statistically significant increase in the mean micronuclei frequency MN.
MDA levels were significantly increased in women with recurrent pregnancy loss when compared to the control group 1. Collectively, these studies highlight the role of oxidative stress OS in recurrent pregnancy loss RPL.
Because generation of reactive oxygen species ROS is the result of the aerobic cellular respiration and ATP production, living systems have developed necessary defense mechanisms against oxygen toxicity to maintain a delicate homeostatic balance between oxidant and antioxidant state.
Antioxidant defense system involves enzymatic and non-enzymatic agents. Ceruloplasmin, transferrin, ferritin and albumin are non-enzymatic antioxidants in the blood plasma [ 54 ]. Natural non-enzymatic antioxidants are represented by vitamin A, vitamin E, vitamin C, polyphenols, uric acid, flavonoids, carotenoids, glutathione, bilirubin and melatonin [ 55 ].
Metallothionein has antioxidant properties because of the presence of the thiol groups —SH and melatonin is effective hydroxyl radical scavenger [ 54 ].
Authors investigating antioxidant enzyme activity in the placenta, demonstrated strong correlation of antioxidant activity with gestational age and oxygen concentration within the placental tissues [ 56 ].
Thus the ensuing conclusion was that at the end of first trimester, establishment of maternal circulation is associated with burst of oxidative stress even in normal pregnancy and has important role in normal placentation [ 56 ].
Increased oxygen concentration and diminished antioxidant capacity will result in impaired or abnormal placentation and early pregnancy failure. In normal pregnancies intervillous circulation is initiated in the peripheral regions of the placenta and is fully established during the second trimester.
In abnormal pregnancies, premature onset of the maternal placental circulation secondary to reduced trophoblastic invasion, induces oxidative damage to the villous trophoblast and is a key factor in early pregnancy loss [ 57 ].
Association of miscarriage and pregnancy with increased oxidative stress was further supported with the results reported by Jenkins et al.
In this study normal term pregnancies were associated with increased superoxide dismutase SOD levels early in the first trimester while miscarriage group had significantly reduced levels of SOD [ 58 ]. Glutathione GSH is hydrosoluble antioxidant and comprises three amino acids: glycine, cysteine and glutamic acid.
It functions in conjunction with glutathione peroxidase GPx , glutathione reductase GR and glutathione oxidase GOx [ 55 ].
Glutathione GSH and glutathione peroxidase GPx are efficient protective antioxidants responsible to maintain redox homeostasis [ 59 ]. The activity of GPx depends on the presence of reduced glutathione GSH , which is major cellular redox buffer in cells and it is oxidized by GPx. Oxidized glutathione GSSG is reduced back to GSH by glutathione reductase GR.
Reported plasma glutathione reductase GR activity was 1. Authors reported a similar reduction of placental GR activity in the RPL group when compared to the healthy controls 0. Placental tissue glutathione GSH levels were also significantly decreased in the recurrent miscarriage group compared to the control group 5.
Al sheik et al. Plasma glutathione peroxidase GPx levels in RPL patients and healthy pregnant women HP were 0. Similar pattern was observed for placental tissue GPx in RPL group and healthy controls 0.
Placental tissue of RPL patients revealed highly significant decreased levels of catalase CAT 0. The glutathione S-transferase GST families are believed to exert a critical role in protection against OS by detoxifying DNA, catechol products and oxidized lipids, generated as a result of oxidative damage [ 61 ].
GST izoenzymes catalyze conjugation of reduced glutathione and act as Selenium-independent GSH peroxidases against organic hydroperoxides [ 62 ].
Studies investigating the relation between the RPL and gene polymorphisms of glutathione S-transferase GST M 1 and T 1 suggest increased risk of RPL in women with GSTM1 null polymorphism [ 63 ].
Therefore, administration of N -acetylcysteine NAC , a source of sulfhydryl SH groups and acetylated precursor of reduced glutathione, appears beneficial in oxidative stress conditions associated with decreased GSH. Evidence suggest clinical benefits of NAC use, in management of idiopathic RPL [ 64 ].
Micronutrients selenium Se , zinc Zn , cooper Cu and manganese Mn are cofactors for the enzymatic antioxidants and have a crucial role in antioxidant defense and ROS scavenge. Zinc, magnesium, cooper and selenium deficiency are associated with pregnancy complications, preeclampsia, premature delivery, fetal growth retardation and low birth weight [ 65 ].
Selenium is incorporated into the glutathione peroxidase, thioredoxin reductases and selenoprotein-P [ 66 ]. Decreased levels of selenium and GPx were previously reported by Desai et al.
In this study red cell selenium levels were A pilot study conducted in India yielded comparable results as the mean red cell selenium levels were significantly lower in the RPL patients Selenium deficiency is associated with reduced antioxidant capacity of GPx [ 69 ].
Similarly the placental tissue selenium levels were significantly lower compared to the control group 9. Yet, literature is inconclusive when it comes to the role of decreased Selenium levels in the etiology of RPL since several studies evaluating Se concentrations reported conflicting results.
Al-Kunani and coauthors observed significant reduction of the mean hair selenium levels in the recurrent miscarriage group compared with the control group 0.
Similar results were reported by Thomas et al. The authors concluded that selenium supplementation in RPL cannot be recommended since the importance of selenium deficiency in recurrent miscarriage has still not been determined [ 71 ].
In deficient or excessive levels it can also act as an prooxidant [ 72 ]. Current data indicate significantly decreased plasma zinc levels in RPL subjects compared to healthy controls 2. Alpha-tocopherol, ascorbic acid, beta carotene, taurine, transferrin, ferritin and ceruloplasmin have antioxidant properties [ 55 ].
Ceruloplasmin and transferrin act by sequestering free iron ions and inhibit hydroxyl radical OH production in the Fenton reaction [ 74 ]. Ferritin is important to maintain intracellular iron balance and acts by binding free iron [ 54 ].
Whereas vitamin C ascorbic acid and vitamin E alpha-tocopherol have important antioxidant properties, Cochrane database systematic review on effectiveness and safety of any vitamin supplementation on the risk of miscarriage, found that antioxidant vitamin supplementation had no effect on early or late miscarriage [ 76 ].
Another emerging field of investigations in the etiology of RPL include angiogenesis and apoptosis-related genes. Studies investigating these genes suggest important role of OS-mediated angiogenesis in aberrant placentation and recurrent pregnancy loss [ 77 , 78 ]. Human placenta has a hemochorial type of placentation.
Vascular and embryonic morphogenesis are a prerequisite for normal development of uteroplacental and fetal circulation [ 79 ]. Vascular endothelial growth factor VEGF and fibroblast growth factor FGF with their respective receptors are major angiogenic factors in fetal and placental angiogenesis [ 80 ].
During early pregnancy expression of VEGF mRNA is greater in fetal placental tissue compared with maternal endometrial tissue. Consequently, inappropriate expression of angiogenic factors may contribute to the impaired placental vascularization and placental dysfunction and appears to be involved in the etiology of infertility and fetal growth retardation [ 80 ].
Angiogenesis is regulated by proangiogenic and antiangiogenic factors and recent evidence indicate that oxidative stress is involved in physiological and pathological angiogenesis.
VEGF-dependent and VEGF-independent signaling pathways of angiogenesis are mediated by oxidative stress [ 81 , 82 ]. Association of RPL with aberrant expression of angiogenesis and apoptosis-related genes was previously reported in several studies [ 77 , 78 ].
Choi et al. Zhu et al. found that microRNA miR expression is upregulated in villi and decidua of recurrent pregnancy loss patients. miR overexpression inhibits placental angiogenesis via VEGF suppression and plays important role in the pathogenesis of RPL [ 83 ].
Aberrant angiogenesis in RPL may be related to VEGF dysregulation including VEGF gene polymorphisms [ 84 ]. He et al. Albeit, the direct relationship between the VEGF and RPL was not established, evidence suggest that reduced VEGF expression in RPL patients can contribute to poor angiogenesis and is related to RPL occurrence [ 77 ].
In a case control study, authors reported lower relative expression of VEGF gene and increased expression of VEGF receptors VEGFR1 and VEGFR2 in the endometrium of women with idiopathic recurrent pregnancy loss compared to the control group.
Also, study group with RPL showed significantly increased serum levels of VEGF when compared to the healthy controls The increased expression of VEGF receptors may act as a compensatory mechanism for the decreased VEGF expression, a speculation which warrants further investigation [ 85 ].
In women with RPL levels of soluble VEGF receptor-1 sFlt-1 and VEGF mRNA in the chorionic samples are significantly increased compared to the control group hence, suggesting that overexpression of VEGFA and FLT1 genes is implicated in the etiology of early recurrent pregnancy loss [ 86 ].
The increased body of evidence associates nitrosative stress with recurrent pregnancy loss RPL. Nitric oxide NO is membrane-soluble free radical synthetized by nitric oxide synthase NOS and demonstrates pathological effect at higher concentrations, in particular when reacting with superoxide to form peroxynitrite.
Peroxynitrites are potentially hazardous because they cause nitrosative modifications of proteins and lipids. Evidence suggest the role of nitrosative stress in RPL patients which is revealed by increased NO levels.
A retrospective case—control study Raffaelli et al. Genetic polymorphisms in the NOS2 promoter, altered gene expression and excessive generation of nitric oxide NO was reported as a risk factor for RPL.
During normal pregnancy NO is involved in maternal vasodilatation, trophoblast invasion, apoptosis and platelet aggregation in the intervillous space [ 89 ]. Yet, NO overproduction will cause p53 protein phosphorylation, apoptosis and impaired placental proliferation [ 90 ].
Endothelium-derived NO act as a physiological mediator of early pregnancy and is involved in the regulation of placental function. Several studies support the concept of polygenetic etiology of RPL. A prospective case—control study investigated women with idiopathic recurrent miscarriage compared to 91 healthy controls and reported a 1.
Although, the association between recurrent miscarriage and NOS3 polymorphism was demonstrated, authors could not specify at what level a lack of eNOS derived NO affects the risk of RPL [ 91 ].
A systematic review and meta-analysis conducted by Su et al. This integrative overview based on the results of previous studies has shown that oxidative and nitrosative stress play an important role in the etiopathogenesis of early pregnancy loss and recurrent pregnancy loss.
Free radicals, reactive oxygen species ROS and reactive nitrogen species RNS are a product of aerobic metabolism. At basal or moderate levels these species have various physiological functions.
Cellular oxidants are involved in the maintenance of redox homeostasis which is necessary for normal physiological functions. They promote natural defenses, contribute to the proliferation and apoptosis depending on signaling and executive pathways, regulate immune response, activate proliferative pathways and exert signaling properties in cell communication.
Imbalance caused by increased generation of free radicals and inefficient antioxidant capacity leads to oxidative stress with subsequent OS-derived damage to nucleic acids, lipids and proteins. Albeit, the currently available studies support the concept that oxidative stress and OS-mediated damage is implicated as an essential factor in the etiology of RPL, exact mechanisms of this interaction remains largely indefinable.
Future studies are required to clarify the limits of the redox window above which ROS become damaging, regulators of placental vascularization and angiogenesis, redox adaptation of the placenta to ensure positive pregnancy outcome, altered expression of antioxidant genes and underlying mechanisms through which OS affects pregnancy outcome.
Exogenous sources of ROS production such as smoking and alcohol consumption are important contributors of oxidative stress and hold the potential for negative impact in maternal and fetal health.
Dietary antioxidants are crucial in maintaining healthy living but data on clinical benefit or positive effects of dietary antioxidant supplementation in pregnancy and female reproductive disease are scarce.
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Ptegnancy Free radicals and pregnancy complications can be affected pregnancu numerous pathologies, from those which are mild Muscle mass evaluation reversible to others which are life-threatening. Oxidative stress is caused by an imbalance between production and Free radicals and pregnancy complications pregnzncy reactive oxygen species ROS in cells and tissues and the ability of a biological system to detoxify these reactive products. In pregnancy, ROS are generated mainly in the placenta, but xanthine oxidase XO are present in the vascular endothelium, and nitric oxide synthase NOS are also sources of ROS. Encyclopedia Scholarly Community. Entry Journal Book Video Image About Entry Entry Video Image. Submitted Successfully! Thank you for your contribution!Video
What are Antioxidants and Free Radicals Anyway?! Reproductive Health Adolescent fat distribution 18Article number: Cite this article. Metrics details. Recent studies prfgnancy that systemic prfgnancy placental oxidative stress OS represents an essential rasicals in African Mango seed triglyceride levels Free radicals and pregnancy complications of RPL. This article is rzdicals comprehensive narrative FFree of Free radicals and pregnancy complications published studies concerning the role of oxidative stress in the etiology of recurrent pregnancy loss. We conducted literature search of published studies in the English language focusing on oxidative stress and its association with recurrent pregnancy loss RPL utilizing the Medline and Cochrane databases from through January The search yielded publications, of which 92 were included in the final analysis. Reactive oxygen species ROS and reactive nitrogen species RNS at basal levels have various physiological functions whereas deviation from redox window is associated with different pathologies including early pregnancy loss.
Die sehr ausgezeichnete Idee
Ja, wirklich.
die Ausgezeichnete Idee und ist termingemäß