Other sources of the SO anion include the short electron chain in the endoplasmic reticulum ER , cytochrome P, and the enzyme nicotinamide adenine dinucleotide phosphate NADPH oxidase, which generates substantial quantities --especially during early pregnancy-- and other oxido-reductases [ 2 , 11 ].

Mitochondria are central to metabolic activities in cells, so any disturbance in their functions can lead to profoundly altered generation of adenine triphosphate ATP. Energy from ATP is essential for gamete functions. Although mitochondria are major sites of ROS production, excessive ROS can affect functions of the mitochondria in oocytes and embryos.

This mitochondrial dysfunction may lead to arrest of cell division, triggered by OS [ 15 , 16 ]. A moderate increase in ROS levels can stimulate cell growth and proliferation, and allows for the normal physiological functions.

Conversely, excessive ROS will cause cellular injury e. The SO anion is detoxified by superoxide dismutase SOD enzymes, which convert it to H 2 O 2. Catalase and glutathione peroxidase GPx further degrade the end-product to water H 2 O. Although H 2 O 2 is technically not a free radical, it is usually referred to as one due to its involvement in the generation and breakdown of free radicals.

By maintaining tissue homeostasis and purging damaged cells, apoptosis plays a key role in normal development. Apoptosis results from overproduction of ROS, inhibition of ETC, decreased antioxidant defenses, and apoptosis-activating proteins, amongst others [ 18 ].

In mammals, RNS are mainly derived from NO, which is formed from O 2 and L-arginine, and its reaction with the SO anion, which forms peroxynitrite [ 2 ]. Peroxynitrite is capable of inducing lipid peroxidation and nitrosation of many tyrosine molecules that normally act as mediators of enzyme function and signal transduction [ 19 ].

Nitric oxide is a free radical with vasodilatory properties and is an important cellular signaling molecule involved in many physiological and pathological processes. Although the vasodilatory effects of NO can be therapeutic, excessive production of RNS can affect protein structure and function, and thus, can cause changes in catalytic enzyme activity, alter cytoskeletal organization, and impair cell signal transduction [ 5 , 11 ].

Oxidative conditions disrupt vasomotor responses [ 20 ] and NO-related effects have also been proposed to occur through ROS production from the interaction between NO and the SO anion [ 21 ].

In the absence of L-arginine [ 19 ] and in sustained settings of low antioxidant status [ 20 ], the intracellular production of the SO anion increases. The elevation of the SO anion levels promotes reactions between itself and NO to generate peroxynitrite, which exacerbates cytotoxicity.

As reviewed by Visioli et al , the compromised bioavailability of NO is a key factor leading to the disruption of vascular functions related to infertile states [ 20 ]. Thus, cell survival is largely dependent on sustained physiological levels of NO [ 22 ].

Within a cell, the actions of NO are dependent on its levels, the redox status of the cell, and the amount of metals, proteins, and thiols, amongst other factors [ 19 ].

The nitric oxide synthase NOS enzyme system catalyzes the formation of NO from O 2 and L-arginine using NADPH as an electron donor [ 24 ] and are comprised of the following isoforms: neuronal NOS nNOS or NOS I , inducible NOS iNOS or NOS II , and endothelial NOS eNOS or NOS III. In general, NO produced by eNOS and nNOS appears to regulate physiologic functions while iNOS production of NO is more active in pathophysiological situations.

The NOS family is encoded by the genes for their isoforms. The nNOS isoform functions as a neurotransmitter and iNOS is expressed primarily in macrophages following induction by cytokines.

The activity of eNOS is increased in response to the luteinizing hormone LH surge and human chorionic gonadotropin hCG [ 11 ]. In normal long-term conditions such as healthy pregnancies, vasodilation is particularly prominent in the uterine vessels [ 28 , 29 ]. Hypoxic conditions also regulate NOS [ 34 ] and enhanced expression of eNOS has been reported in ovine uterine arteries in response to chronic hypoxia [ 35 ].

Conversely, suboptimal vascular endothelial production of NO has been shown to cause hypertension not only in eNOS knockout mice [ 36 , 37 ], but more importantly, in humans [ 38 ]. Furthermore, failure of pregnancy states to adapt to sustained vasodilation [ 20 ] induced by the CCE signaling response can lead to complications such as IUGR [ 28 ] and preeclampsia, in which hypertension could be fatal [ 30 ].

There are two types of antioxidants: enzymatic and non-enzymatic. Enzymatic antioxidants possess a metallic center, which gives them the ability to take on different valences as they transfer electrons to balance molecules for the detoxification process.

They neutralize excess ROS and prevent damage to cell structures. Endogenous antioxidants enzymes include SOD, catalase, GPx, and glutathione oxidase. Dismutation of the SO anion to H 2 O 2 by SOD is fundamental to anti-oxidative reactions.

The enzyme SOD exists as three isoenzymes [ 11 ]: SOD 1, SOD 2, and SOD 3. SOD 1 contains Cu and zinc Zn as metal co-factors and is located in the cytosol. SOD 2 is a mitochondrial isoform containing manganese Mn , and SOD 3 encodes the extracellular form. SOD 3 is structurally similar to Cu,Zn-SOD, as it contains Cu and Zn as cofactors.

The glutathione GSH family of enzymes includes GPx, GST, and GSH reductase. Depletion of GSH results in DNA damage and increased H 2 O 2 concentrations; as such, GSH is an essential antioxidant. During the reduction of H 2 O 2 to H 2 Oand O 2 , GSH is oxidized to GSSG by GPx.

Glutathione reductase participates in the reverse reaction, and utilizes the transfer of a donor proton from NADPH to GSSG, thus, recycling GSH [ 39 ]. Glutathione peroxidase exists as five isoforms in the body: GPx1, GPx2, GPx3, GPx4 [ 11 ], and GPx5 [ 39 ].

GPx1 is the cytosolic isoform that is widely distributed in tissues, while GPx2 encodes a gastrointestinal form with no specific function; GPx3 is present in plasma and epididymal fluid.

GPx 4 specifically detoxifies phospholipid hydroperoxide within biological membranes. Vitamin E α-tocopherol protects GPx4-deficient cells from cell death [ 40 ]. GPx5 is found in the epididymis [ 39 ]. Glutathione is the major thiol buffer in cells, and is formed in the cytosol from cysteine, glutamate, and glycine.

Its levels are regulated through its formation de-novo, which is catalyzed by the enzymes γ-glutamylcysteine synthetase and glutathione synthetase [ 4 , 11 ]. In cells, GSH plays multiple roles, which include the maintenance of cells in a reduced state and formation of conjugates with some hazardous endogenous and xenobiotic compounds.

The non-enzymatic antioxidants consist of dietary supplements and synthetic antioxidants such as vitamin C, GSH, taurine, hypotaurine, vitamin E, Zn, selenium Se , beta-carotene, and carotene [ 41 ]. Vitamin C ascorbic acid is a known redox catalyst that can reduce and neutralize ROS.

Its reduced form is maintained through reactions with GSH and can be catalyzed by protein disulfide isomerase and glutaredoxins. Glutathione is a peptide found in most forms of aerobic life as it is made in the cytosol from cysteine, glutamate, and glycine [ 42 ]; it is also the major non-enzymatic antioxidant found in oocytes and embryos.

Its antioxidant properties stem from the thiol group of its cysteine component, which is a reducing agent that allows it to be reversibly oxidized and reduced to its stable form [ 42 ]. Levels of GSH are regulated by its formation de-novo, which is catalyzed by the enzymes gamma-GCS and glutathione synthetase [ 4 , 11 ].

Glutathione participates in reactions, including the formation of glutathione disulfide, which is transformed back to GSH by glutathione reductase at the expense of NADPH [ 17 ].

Cysteine and cysteamine CSH increase the GSH content of the oocyte. Cysteamine also acts as a scavenger and is an antioxidant essential for the maintenance of high GSH levels.

Furthermore, CSH can be converted to another antioxidant, hypotaurine [ 43 , 44 ]. The concentrations of many amino acids, including taurine, fluctuate considerably during folliculogenesis. Taurine and hypotaurine are scavengers that help maintain redox homeostasis in gametes.

Both neutralize lipid peroxidation products, and hypotaurine further neutralizes hydroxyl radicals [ 44 ]. Like GSH, the Thioredoxin Trx system regulates gene functions and coordinates various enzyme activities.

It detoxifies H 2 O 2 and converts it to its reduced state via Trx reductase [ 45 ]. Normally, Trx is bound to apoptosis-regulating signal kinase ASK 1, rendering it inactive.

However, when the thiol group of Trx is oxidized by the SO anion, ASK1 detaches from Trx and becomes active leading to enhanced apoptosis. ASK1 can also be activated by exposure to H 2 O 2 or hypoxia-reoxygenation, and inhibited by vitamins C and E [ 2 ].

The Trx system also plays a role in female reproduction and fetal development by being involved in cell growth, differentiation, and death. Vitamin E α-tocopherol is a lipid soluble vitamin with antioxidant activity. It consists of eight tocopherols and tocotrienols. It plays a major role in antioxidant activities because it reacts with lipid radicals produced during lipid peroxidation [ 42 ].

This reaction produces oxidized α-tocopheroxyl radicals that can be transformed back to the active reduced form by reacting with other antioxidants like ascorbate, retinol, or ubiquinol. The hormone melatonin is an antioxidant that, unlike vitamins C and E and GSH, is produced by the human body.

In contrast to other antioxidants, however, melatonin cannot undergo redox cycling; once it is oxidized, melatonin is unable to return to its reduced state because it forms stable end-products after the reaction occurs.

Transferrin and ferritin, both iron-binding proteins, play a role in antioxidant defense by preventing the catalyzation of free radicals through chelation [ 46 ].

Nutrients such as Se, Cu, and Zn are required for the activity of some antioxidant enzymes, although they have no antioxidant action themselves. Oxidative stress occurs when the production of ROS exceeds levels of antioxidants and can have damaging effects on both male and female reproductive abilities.

However, it should be recalled that OS is also considered a normal physiological state, which is essential for many metabolic processes and biological systems to promote cell survival. Redox states of oocyte and embryo metabolism are heavily determined by ETs that lead to oxidation or reduction, and are thus termed redox reactions [ 18 ].

Significant sources of ROS in Graffian follicles include macrophages, neutrophils, and granulosa cells. During folliculogenesis, oocytes are protected from oxidative damage by antioxidants such as catalase, SOD, glutathione transferase, paraoxanase, heat shock protein HSP 27, and protein isomerase [ 47 ].

Once assembled, ROS are capable of reacting with other molecules to disrupt many cellular components and processes. The continuous production of ROS in excess can induce negative outcomes of many signaling processes [ 18 ]. Reactive oxygen species do not always directly target the pathway; instead, they may produce abnormal outcomes by acting as second messengers in some intermediary reactions [ 48 ].

Damage induced by ROS can occur through the modulation of cytokine expression and pro-inflammatory substrates via activation of redox-sensitive transcription factors AP-1, p53, and NF-kappa B.

Under stable conditions, NF-kappa B remains inactive by inhibitory subunit I-kappa B. The increase of pro-inflammatory cytokines interleukin IL 1-beta and tumor necrosis factor TNF -alpha activates the apoptotic cascade, causing cell death.

Conversely, the antioxidants vitamin C and E, and sulfalazine can prevent this damage by inhibiting the activation of NF-kappa B [ 3 ]. Deleterious attacks from excess ROS may ultimately end in cell death and necrosis.

These harmful attacks are mediated by the following more specialized mechanisms [ 2 ]. Consequently, the mitochondrial membrane potential becomes unstable and ATP production ceases.

Lipid peroxidation : This occurs in areas where polyunsaturated fatty acid side chains are prevalent. Vitamin E can break this chain reaction due to its lipid solubility and hydrophobic tail. Protein modifications : Amino acids are targets for oxidative damage. Direct oxidation of side chains can lead to the formation of carbonyl groups.

DNA oxidation : Mitochondrial DNA is particularly prone to ROS attack due to the presence of O 2 - in the ETC, lack of histone protection, and absence of repair mechanisms. Reactive oxygen species are known to promote tyrosine phosphorylation by heightening the effects of tyrosine kinases and preventing those of tyrosine phosphatases.

The inhibition of tyrosine phosphatases by ROS takes place at the cysteine residue of their active site. One possible mechanism of this inhibition is that it occurs through the addition of H 2 O 2 , which binds the cysteine residue and converts it to sulfenic acid.

Another possible mechanism of inhibition is through the production of GSH via reduction from its oxidized form of GSSG; this conversion alters the catalytic cysteine residue site [ 49 ]. The human body is composed of many important signaling pathways.

Amongst the most important signaling pathways in the body are the mitogen-activated protein kinases MAPK. MAPK pathways are major regulators of gene transcription in response to OS. This process promotes the actions of receptor tyrosine kinases, protein tyrosine kinases, receptors of cytokines, and growth factors [ 50 , 51 ].

Excessive amounts of ROS can disrupt the normal effects of these cascade-signaling pathways. Other pathways that can be activated by ROS include the c-Jun N -terminal kinases JNK and p38 pathways. The JNK pathway prevents phosphorylation due to its inhibition by the enzyme GST.

The addition of H 2 O 2 to this cascade can disrupt the complex and promote phosphorylation [ 52 , 53 ]. The presence of ROS can also dissociate the ASK1—Trx complex by activating the kinase [ 54 ] through the mechanism discussed earlier. Hypoxia-inducible factors HIF are controlled by O 2 concentration.

They are essential for normal embryonic growth and development. Low O 2 levels can alter HIF regulatory processes by activating erythropoietin, another essential factor for proper embryonic growth and development [ 55 , 56 ]. The preservation of physiological cellular functions depends on the homeostatic balance between oxidants and antioxidants.

Oxidative stress negatively alters cell-signaling mechanisms, thereby disrupting the physiologic processes required for cell growth and proliferation.

Almost half of infertility cases are caused by male reproductive pathologies [ 57 ], which can be congenital or acquired. Both types of pathology can impair spermatogenesis and fertility [ 58 , 59 ].

In males, the role of OS in pathologies has long been recognized as a significant contributor to infertility. Men with high OS levels or DNA damaged sperm are likely to be infertile [ 60 ]. The key predictors of fertilization capability are sperm count and motility.

These essential factors can be disturbed by ROS [ 60 ] and much importance has been given to OS as a major contributor to infertility in males [ 61 ]. Low levels of ROS are necessary to optimize the maturation and function of spermatozoa. The main sources of seminal ROS are immature spermatozoa and leukocytes [ 4 ].

In addition, acrosome reactions, motility, sperm capacitation, and fusion of the sperm membrane and the oolemma are especially dependent on the presence of ROS [ 4 , 60 ]. Abnormal and non-viable spermatozoa can generate additional ROS and RNS, which can disrupt normal sperm development and maturation and may even result in apoptosis [ 4 ].

Specifically, H 2 O 2 and the SO anion are perceived as main instigators of defective sperm functioning in infertile males [ 60 ]. Abnormally high seminal ROS production may alter sperm motility and morphology, thus impairing their capacity to fertilize [ 62 ].

The contribution of OS to male infertility has been well documented and extensively studied. On the other hand, the role of OS in female infertility continues to emerge as a topic of interest, and thus, the majority of conducted studies provide indirect and inconclusive evidence regarding the oxidative effects on female reproduction.

Each month, a cohort of oocytes begin to grow and develop in the ovary, but meiosis I resumes in only one of them, the dominant oocyte. This process is targeted by an increase in ROS and inhibited by antioxidants.

In contrast, the progression of meiosis II is promoted by antioxidants [ 42 ], suggesting that there is a complex relationship between ROS and antioxidants in the ovary.

The increase in steroid production in the growing follicle causes an increase in P, resulting in ROS formation. Reactive oxygen species produced by the pre-ovulatory follicle are considered important inducers for ovulation [ 4 ].

Oxygen deprivation stimulates follicular angiogenesis, which is important for adequate growth and development of the ovarian follicle. Follicular ROS promotes apoptosis, whereas GSH and follicular stimulating hormone FSH counterbalance this action in the growing follicle. Estrogen increases in response to FSH, triggering the generation of catalase in the dominant follicle, and thus avoiding apoptosis [ 42 ].

Ovulation is essential for reproduction and commences by the LH surge, which promotes important physiological changes that result in the release of a mature ovum. An overabundance of post-LH surge inflammatory precursors generates ROS; on the other hand, depletion of these precursors impairs ovulation [ 46 ].

In the ovaries, the corpus luteum is produced after ovulation; it produces progesterone, which is indispensable for a successful pregnancy. Reactive oxygen species are also produced in the corpus luteum and are key factors for reproduction.

When pregnancy does not occur, the corpus luteum regresses. Conversely, when pregnancy takes place, the corpus luteum persists [ 63 ]. A rapid decline in progesterone is needed for adequate follicle development in the next cycle.

Cu,Zn-SOD increases in the corpus luteum during the early to mid-luteal phase and decreases during the regression phase. This activity parallels the change in progesterone concentration, in contrast to lipid peroxide levels, which increase during the regression phase. The decrease in Cu,Zn-SOD concentration could explain the increase in ROS concentration during regression.

Other possible explanations for decreased Cu,Zn-SOD are an increase in prostaglandin PG F2-alpha or macrophages, or a decrease in ovarian blood flow [ 42 ]. Prostaglandin F2-alpha stimulates production of the SO anion by luteal cells and phagocytic leukocytes in the corpus luteum.

Decreased ovarian blood flow causes tissue damage by ROS production. Concentrations of Mn-SOD in the corpus luteum during regression increase to scavenge the ROS produced in the mitochondria by inflammatory reactions and cytokines.

Complete disruption of the corpus luteum causes a substantial decrease of Mn-SOD in the regressed cell. At this point, cell death is imminent [ 46 ]. The Cu,Zn-SOD enzyme is intimately related to progesterone production, while Mn-SOD protects luteal cells from OS-induced inflammation [ 42 ].

During normal pregnancy, leukocyte activation produces an inflammatory response, which is associated with increased production of SO anions in the 1 st trimester [ 64 , 65 ]. Importantly, OS during the 2 nd trimester of pregnancy is considered a normal occurrence, and is supported by mitochondrial production of lipid peroxides, free radicals, and vitamin E in the placenta that increases as gestation progresses [ 66 — 69 ].

Aging is defined as the gradual loss of organ and tissue functions. Oocyte quality decreases in relation to increasing maternal age. Recent studies have shown that low quality oocytes contain increased mtDNA damage and chromosomal aneuploidy, secondary to age-related dysfunctions.

These mitochondrial changes may arise from excessive ROS, which occurs through the opening of ion channels e. Levels of 8-oxodeoxyguanosine 8-OHdG , an oxidized derivative of deoxyguanosine, are higher in aging oocytes.

In fact, 8-OHdG is the most common base modification in mutagenic damage and is used as a biomarker of OS [ 70 ]. Oxidative stress, iron stores, blood lipids, and body fat typically increase with age, especially after menopause. The cessation of menses leads to an increase in iron levels throughout the body.

Elevated iron stores could induce oxidative imbalance, which may explain why the incidence of heart disease is higher in postmenopausal than premenopausal women [ 71 ].

Menopause also leads to a decrease in estrogen and the loss of its protective effects against oxidative damage to the endometrium [ 72 ]. Hormone replacement therapy HRT may be beneficial against OS by antagonizing the effects of lower antioxidant levels that normally occurs with aging.

However, further studies are necessary to determine if HRT can effectively improve age-related fertility decline. Endometriosis is a benign, estrogen-dependent, chronic gynecological disorder characterized by the presence of endometrial tissue outside the uterus.

Lesions are usually located on dependent surfaces in the pelvis and most often affect the ovaries and cul-de-sac. They can also be found in other areas such as the abdominal viscera, the lungs, and the urinary tract. These may include retrograde menstruation, impaired immunologic response, genetic predisposition, and inflammatory components [ 74 ].

The mechanism that most likely explains pelvic endometriosis is the theory of retrograde menstruation and implantation. This theory poses that the backflow of endometrial tissue through the fallopian tubes during menstruation explains its extra-tubal locations and adherence to the pelvic viscera [ 75 ].

Studies have reported mixed results regarding detection of OS markers in patients with endometriosis. While some studies failed to observe increased OS in the peritoneal fluid or circulation of patients with endometriosis [ 76 — 78 ], others have reported increased levels of OS markers in those with the disease [ 79 — 83 ].

The peritoneal fluid of patients have been found to contain high concentrations of malondialdehyde MDA , pro-inflammatory cytokines IL-6, TNF-alpha, and IL-beta , angiogenic factors IL-8 and VEGF , monocyte chemoattractant protein-1 [ 82 ], and oxidized LDL ox-LDL [ 84 ].

Pro-inflammatory and chemotactic cytokines play a central role in the recruitment and activation of phagocytic cells, which are the main producers of both ROS and RNS [ 82 ]. Non-enzymatic peroxidation of arachidonic acid leads to the production of F2-isoprostanes [ 85 ].

Lipid peroxidation, and thus, OS in vivo [ 83 ], has been demonstrated by increased levels of the biomarker 8-iso-prostaglandin F2-alpha 8-iso-PGF2-alpha [ 86 — 88 ]. Along with its vasoconstrictive properties, 8-iso-PGF2-alpha promotes necrosis of endothelial cells and their adhesion to monocytes and polymorphonuclear cells [ 89 ].

A study by Sharma et al measured peritoneal fluid and plasma levels of 8-iso-PGF2-alpha in vivo of patients with endometriosis. They found that 8-iso-PGF2-alpha levels in both the urine and peritoneal fluid of patients with endometriosis were significantly elevated when compared with those of controls [ 83 ].

Levels of 8-iso-PGF2-alpha are likely to be useful in predicting oxidative status in diseases such as endometriosis, and might be instrumental in determining the cause of concurrent infertility.

The main inducible forms of HSP70 are HSPA1A and HSPA1B [ 91 ], also known as HSP70A and HSP70 B respectively [ 90 ]. Both forms have been reported as individual markers of different pathological processes [ 92 ].

Heat shock protein 70 B is an inducible member of HSP family that is present in low levels under normal conditions [ 93 ] and in high levels [ 94 ] under situations of stress. It functions as a chaperone for proteostatic processes such as folding and translocation, while maintaining quality control [ 95 ].

It has also been noted to promote cell proliferation through the suppression of apoptosis, especially when expressed in high levels, as noted in many tumor cells [ 94 , 96 — 98 ]. As such, HSP70 is overexpressed when there is an increased number of misfolded proteins, and thus, an overabundance of ROS [ 94 ].

The release of HSP70 during OS stimulates the expression of inflammatory cytokines [ 93 , 99 ] TNF-alpha, IL-1 beta, and IL-6, in macrophages through toll-like receptors e. TLR 4 , possibly accounting for pelvic inflammation and growth of endometriotic tissue [ 99 ]. Fragmentation of HSP70 has been suggested to result in unregulated expression of transcription factor NF-kappa B [ ], which may further promote inflammation within the pelvic cavity of patients with endometriosis.

Oxidants have been proposed to encourage growth of ectopic endometrial tissue through the induction of cytokines and growth factors [ ]. Signaling mediated by NF-kappa B stimulates inflammation, invasion, angiogenesis, and cell proliferation; it also prevents apoptosis of endometriotic cells.

Activation of NF-kappa B by OS has been detected in endometriotic lesions and peritoneal macrophages of patients with endometriosis [ ]. N-acetylcysteine NAC and vitamin E are antioxidants that limit the proliferation of endometriotic cells [ ], likely by inhibiting activation of NF-kappa B [ ].

Future studies may implicate a therapeutic effect of NAC and vitamin E supplementation on endometriotic growth. This may explain the increased expressions of these proteins in ectopic versus eutopic endometrial tissue [ ].

Iron mediates production of ROS via the Fenton reaction and induces OS [ ]. In the peritoneum of patients with endometriosis, accumulation of iron and heme around endometriotic lesions [ ] from retrograde menstruation [ ] up-regulates iNOS activity and generation of NO by peritoneal macrophages [ ].

Extensive degradation of DNA by iron and heme accounts for their considerable free radical activity. Chronic oxidative insults from iron buildup within endometriotic lesions may be a key factor in the development of the disease [ ].

Naturally, endometriotic cysts contain high levels of free iron as a result of recurrent cyclical hemorrhage into them compared to other types of ovarian cysts. However, high concentrations of lipid peroxides, 8-OHdG, and antioxidant markers in endometrial cysts indicate lipid peroxidation, DNA damage, and up-regulated antioxidant defenses respectively.

These findings strongly suggest altered redox status within endometrial cysts [ ]. Potential therapies have been suggested to prevent iron-stimulated generation of ROS and DNA damage.

Based on results from their studies of human endometrium, Kobayashi et al have proposed a role for iron chelators such as dexrazoxane, deferoxamine, and deferasirox to prevent the accumulation of iron in and around endometriotic lesions [ ].

Future studies investigating the use of iron chelators may prove beneficial in the prevention of lesion formation and the reduction of lesion size. Many genes encoding antioxidant enzymes and proteins are recruited to combat excessive ROS and to prevent cell damage. Amongst these are Trx and Trx reductase, which sense altered redox status and help maintain cell survival against ROS [ ].

Total thiol levels, used to predict total antioxidant capacity TAC , have been found to be decreased in women with pelvic endometriosis and may contribute to their status of OS [ 81 , ]. Conversely, results from a more recent study failed to correlate antioxidant nutrients with total thiol levels [ ].

Patients with endometriosis tend to have lower pregnancy rates than women without the disease. Low oocyte and embryo quality in addition to spermatotoxic peritoneal fluid may be mediated by ROS and contribute to the subfertility experienced by patients with endometriosis [ ].

The peritoneal fluid of women with endometriosis contains low concentrations of the antioxidants ascorbic acid [ 82 ] and GPx [ 81 ]. The reduction in GPx levels was proposed to be secondary to decreased progesterone response of endometrial cells [ ]. The link between gene expression for progesterone resistance and OS may facilitate a better understanding of the pathogenesis of endometriosis.

It has been suggested that diets lacking adequate amounts of antioxidants may predispose some women to endometriosis [ ]. Studies have shown decreased levels of OS markers in people who consume antioxidant rich diets or take antioxidant supplements [ — ].

In certain populations, women with endometriosis have been observed to have a lower intake of vitamins A, C [ ], E [ — ], Cu, and Zn [ ] than fertile women without the disease [ — ].

Daily supplementation with vitamins C and E for 4 months was found to decrease levels of OS markers in these patients, and was attributed to the increased intake of these vitamins and their possible synergistic effects.

Pregnancy rates, however, did not improve [ ]. Intraperitoneal administration of melatonin, a potent scavenger of free radicals, has been shown to cause regression of endometriotic lesions [ — ] by reducing OS [ , ]. These findings, however, were observed in rodent models of endometriosis, which may not closely resemble the disease in humans.

It is evident that endometriotic cells contain high levels of ROS; however, their precise origins remain unclear. Impaired detoxification processes lead to excess ROS and OS, and may be involved in increased cellular proliferation and inhibition of apoptosis in endometriotic cells.

It is a disorder characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovaries [ ]. Clinical manifestations of PCOS commonly include menstrual disorders, which range from amenorrhea to menorrhagia. Skin disorders are also very prevalent amongst these women.

Insulin resistance may be central to the etiology of PCOS. Signs of insulin resistance such as hypertension, obesity, and central fat distribution are associated with other serious conditions, such as metabolic syndrome, nonalcoholic fatty liver [ ], and sleep apnea.

All of these conditions are risk factors for long-term metabolic sequelae, such as cardiovascular disease and diabetes [ ].

Most importantly, waist circumference, independent of body mass index BMI , is responsible for an increase in oxLDL [ 71 ]. Polycystic ovary syndrome is also associated with decreased antioxidant concentrations, and is thus considered an oxidative state [ ]. The decrease in mitochondrial O 2 consumption and GSH levels along with increased ROS production explains the mitochondrial dysfunction in PCOS patients [ ].

The mononuclear cells of women with PCOS are increased in this inflammatory state [ ], which occurs more so from a heightened response to hyperglycemia and C-reactive protein CRP.

Physiological hyperglycemia generates increased levels of ROS from mononuclear cells, which then activate the release of TNF-alpha and increase inflammatory transcription factor NF-kappa B. As a result, concentrations of TNF-alpha, a known mediator of insulin resistance, are further increased.

The resultant OS creates an inflammatory environment that further increases insulin resistance and contributes to hyperandrogenism [ ]. Lifestyle modification is the cornerstone treatment for women with PCOS.

Immune cells referred to as macrophages which produce free radicals while fighting off invading germs. These free radicals can harm healthy cells, leading to inflammation.

Under normal circumstances, inflammation goes away after the immune system eliminates the infection or repairs the damaged tissue. However, oxidative stress can also trigger the inflammatory response, which, in turn, produces more free radicals which can lead to further oxidative stress, creating a cycle.

Chronic inflammation due to oxidative stress may lead to numerous conditions, including diabetes, cardiovascular disease and arthritis. It is important to remember that the body requires both free radicals and antioxidants. Having too many or too few of either may cause health problems.

Lifestyle and nutritional measures that may help reduce oxidative stress in the body include:. Eating five servings per day of a variety of fruits and vegetables is the best way to provide your body what it needs to produce antioxidants.

Examples of fruits and vegetables include:. Copyright: © The Authors. This is an open access article under the terms of the Creative Commons Attribution NonCommercial ShareAlike 4.

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Free radicals may generate a massive chain of chemical events in your body because they combine so readily with other substances.

These processes are termed oxidation. They may be helpful or dangerous. Antioxidants are compounds that can give an electron to a free radical without rendering themselves unstable.

This allows the free radical to stabilise and become less reactive. You might think of oxidation as the process through which your body converts oxygen into energy, fights off illness, etc. The reactive oxygen species you breathe produce free radicals, which are liberated atoms.

Each time an atom of oxygen is broken down and utilised by the body, it releases one unpaired electron. These atoms seek a pair of electrons as they roam the body searching for one to pair with.

Cells, proteins, and DNA are all harmed as a result. Free radicals have been shown to damage DNA and mucous membranes directly. Cigarettes, air pollution, and toxins in our daily life are all potential sources of free radicals in addition to cellular energy generation.

Oxidative Stress has been related to the development of several diseases, including cancer, heart failure, and diabetes. Unfortunately, free radical damage is what causes ageing in the first place. The antioxidants may neutralise these free radicals in your cells, which help keep be affected by several variables, including:.

To be sure, this will lead to oxidative stress. Depending on the degree, inflammation can be either short-lived or long-lasting.

The following are the most typical causes of chronic inflammation:. Inflammation in the body is also caused by several lifestyle factors such as excessive drinking, chronic stress, excessive smoking etc.

Inflammation does not go away on its own. Dietary changes can be made to improve the health of people. The risk of a wide range of diseases can be reduced by eating a nutritious, disease-preventing diet rich in anti-inflammatory foods. Unchecked oxidative Stress may be harmful to your health.

Many of us cannot have a healthy immune system or a recuperation system that works effectively. However, chronic inflammatory disorders such as arthritis may be uncomfortable and have a terrible influence on your overall health, even if inflammation is present in proper proportions.

While free radicals are wreaking havoc on your body, a few simple lifestyle modifications may dramatically lessen the damage they do. In this manner: To begin, ensure that your food is rich in antioxidants.

Including a wide variety of fruits and vegetables in your diet may offer your body the antioxidant phytochemicals it needs to make its antioxidants and the antioxidants themselves. Numerous illnesses of the renal apparatus, such as glomerular- and tubulointerstitial nephritis, renal failure, proteinuria, and uremia, are linked to oxidative stress.

Oxidative Stress is detrimental to renal function because ROS generation activates inflammatory cells and the synthesis of cytokines, leading to a pre-inflammation state in the kidney.

Several researchers have suggested that oxidative stress might be a factor in delayed sexual development and puberty onset. The same metallic element, Cd, has been linked to increased free radicals and oxidative stress in children and pregnant women in the prepubertal stage of life.

We may conclude that oxidative Stress and free radicals are implicated in a wide range of clinical diseases that impact a variety of tissues and systems, making them one of the most significant and ubiquitous threats to human health.

Oxidative Stress has been related to several lung disorders, including asthma and COPD, characterised by persistent inflammation. One of the most well-known ways oxidants contribute to inflammation is via the activation of kinases linked to various pathways and transcription factors.

Macrophages and activated T cells infiltrate the joints and surrounding tissues in rheumatoid arthritis, a chronic inflammatory condition. It has been shown that elevated levels of isoprostane and prostaglandin in the synovial fluid of individuals with this syndrome suggest the importance of free radicals present at sites of inflammation in the onset and evolution of this condition.

Multifactorial aetiology characterises cardiovascular diseases CVDs , which have many risk factors, including high cholesterol, high blood pressure, tobacco use, diabetes, an imbalanced diet, and a sedentary lifestyle. Select your language of interest to view the total content in your interested language.

Oxidants and Antioxidants in Medical Science received citations as per google scholar report. Mucahit Avcil, Department of Emergency Medicine, Adnan Menderes University, Aydan, Turkey, Email: muc. avilhit gmail. Received: Feb, Manuscript No.

EJMOAMS; Editor assigned: Feb, Pre QC No. EJMOAMS PQ ; Reviewed: Feb, QC No. EJMOAMS; Revised: Feb, Manuscript No. EJMOAMS R ; Published: Mar Oxidative stress is basically an imbalance among the production of free radicals and the capacity of the body to counteract or detoxify their dangerous outcomes via neutralization with the aid of using antioxidants.

Oxidative stress results in many pathophysiological conditions inside the body. Oxidative stress is an imbalance of free radicals and antioxidants in the body, which can lead to cell and tissue damage.

Oxidative stress occurs naturally and plays a role in the aging process. However, cells additionally produce antioxidants that neutralize those free radicals.

In general, the body is able to maintain a balance among antioxidants and free radicals. Several factors contribute to oxidative stress and excess free radical production. These factors can include:. This type of oxidative stress causes mild inflammation that goes away after the immune system fights off an infection or repairs an injury.

Uncontrolled oxidative stress can boost up the aging process and may contribute to the development of a number of conditions.

For example, oxidative stress that effects from physical activity may have beneficial, regulatory effects at the body. Exercise will increase free radical formation, which can cause temporary oxidative stress in the muscles.

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Medical News Today. Health Conditions Health Products Discover Tools Connect. How does oxidative stress affect the body? Medically reviewed by Stacy Sampson, D.

What is it? Free radicals Antioxidants Effects Conditions Risk factors Prevention Summary Oxidative stress is an imbalance of free radicals and antioxidants in the body, which can lead to cell and tissue damage.

What is oxidative stress? Share on Pinterest Many lifestyle factors can contribute to oxidative stress. Healthy aging resources To discover more evidence-based information and resources for healthy aging, visit our dedicated hub. Was this helpful? What are free radicals?

What are antioxidants? Share on Pinterest Fresh berries and other fruits contain antioxidants. Effects of oxidative stress. Conditions linked to oxidative stress. Risk factors for oxidative stress. How we reviewed this article: Sources. Medical News Today has strict sourcing guidelines and draws only from peer-reviewed studies, academic research institutions, and medical journals and associations.

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RSV vaccine errors in babies, pregnant people: Should you be worried? This uneven number of electrons allows free radicals to react easily with other molecules. Free radicals can cause large chain chemical reactions in your body because they react so easily with other molecules.

These reactions are called oxidation. They can be beneficial or harmful. Antioxidants are molecules that can donate an electron to a free radical without making themselves unstable. This causes the free radical to stabilize and become less reactive.

Read on to learn how oxidative stress affects the body and how to manage and prevent this imbalance. Oxidation is a normal and necessary process that takes place in your body.

When functioning properly, free radicals can help fight off pathogens. Pathogens lead to infections. When there are more free radicals present than can be kept in balance by antioxidants, the free radicals can start doing damage to fatty tissue, DNA, and proteins in your body.

Proteins, lipids, and DNA make up a large part of your body, so that damage can lead to a vast number of diseases over time. These include:. Everyone produces some free radicals naturally in their body through processes like exercise or inflammation.

However, there are things you can do to minimize the effects of oxidative stress on your body. The main thing you can do is to increase your levels of antioxidants and decrease your formation of free radicals. Eating five servings per day of a variety of fruits and vegetables is the best way to provide your body what it needs to produce antioxidants.

Examples of fruits and vegetables include:. Other healthy lifestyle choices can also prevent or reduce oxidative stress. Here are some lifestyle choices that will help:. Oxidative stress can cause damage to many of your tissues, which can lead to a number of diseases over time.

The antioxidants may neutralise these free radicals in your cells, which help keep be affected by several variables, including:.

To be sure, this will lead to oxidative stress. Depending on the degree, inflammation can be either short-lived or long-lasting. The following are the most typical causes of chronic inflammation:. Inflammation in the body is also caused by several lifestyle factors such as excessive drinking, chronic stress, excessive smoking etc.

Inflammation does not go away on its own. Dietary changes can be made to improve the health of people. The risk of a wide range of diseases can be reduced by eating a nutritious, disease-preventing diet rich in anti-inflammatory foods. Unchecked oxidative Stress may be harmful to your health.

Many of us cannot have a healthy immune system or a recuperation system that works effectively. However, chronic inflammatory disorders such as arthritis may be uncomfortable and have a terrible influence on your overall health, even if inflammation is present in proper proportions.

While free radicals are wreaking havoc on your body, a few simple lifestyle modifications may dramatically lessen the damage they do. In this manner: To begin, ensure that your food is rich in antioxidants. Including a wide variety of fruits and vegetables in your diet may offer your body the antioxidant phytochemicals it needs to make its antioxidants and the antioxidants themselves.

Numerous illnesses of the renal apparatus, such as glomerular- and tubulointerstitial nephritis, renal failure, proteinuria, and uremia, are linked to oxidative stress. Oxidative Stress is detrimental to renal function because ROS generation activates inflammatory cells and the synthesis of cytokines, leading to a pre-inflammation state in the kidney.

Several researchers have suggested that oxidative stress might be a factor in delayed sexual development and puberty onset. The same metallic element, Cd, has been linked to increased free radicals and oxidative stress in children and pregnant women in the prepubertal stage of life.

We may conclude that oxidative Stress and free radicals are implicated in a wide range of clinical diseases that impact a variety of tissues and systems, making them one of the most significant and ubiquitous threats to human health.

Oxidative Stress has been related to several lung disorders, including asthma and COPD, characterised by persistent inflammation. One of the most well-known ways oxidants contribute to inflammation is via the activation of kinases linked to various pathways and transcription factors.

Macrophages and activated T cells infiltrate the joints and surrounding tissues in rheumatoid arthritis, a chronic inflammatory condition.

It has been shown that elevated levels of isoprostane and prostaglandin in the synovial fluid of individuals with this syndrome suggest the importance of free radicals present at sites of inflammation in the onset and evolution of this condition.

Multifactorial aetiology characterises cardiovascular diseases CVDs , which have many risk factors, including high cholesterol, high blood pressure, tobacco use, diabetes, an imbalanced diet, and a sedentary lifestyle. Many CVDs may have oxidative Stress as a significant or secondary cause, according to studies published in the previous few years.