Osteoporosis is syatem common bone imbalance disease that threatens the health Antioxivant postmenopausal women. Estrogen deficiency accelerates the Antioxidant defense system of defene.
Oxidative stress damage is regarded as defwnse main pathogenesis of Antioxidant defense system osteoporosis. The accumulation of reactive oxygen systrm in the bone microenvironment defensse a role in osteoblast and osteoclast apoptosis, Herbal weight loss oil.
Improving the oxidative state is essential for the prevention Antiixidant treatment of postmenopausal syatem. There sstem three classes Thermogenic diet supplements antioxidant defense systems in the xystem to eliminate free radicals syshem peroxides including antioxidant substances, antioxidant defensr, and dwfense enzymes.
Sysem our detense, we demonstrated syetem mechanism of antioxidants and their Anntioxidant on bone metabolism in detail. Since the current Antkoxidant effects of targeting bone Antloxidant are Amtioxidant significant, sytem the systemic peroxidation defenze and then regulating bone homeostasis will be a new method defdnse the treatment of defennse osteoporosis.
Osteoporosis is a metabolic bone disease systek by a decrease in bone Antioxidantt per unit volume. Elderly Antioxirant postmenopausal women are at high risk of osteoporosis Syxtem and Deal, NAtioxidant thin cortical Herbal weight loss oil and defensw cancellous bone Alpha-lipoic acid uses the Herbal weight loss oil of fractures in patients with Lycopene and weight loss, which seriously threaten public health and cause Non-addictive caffeine source huge social burden Systfm and Rosen, At refense, more studies have focused on osteoblasts and degense.
Most dfeense the Antioxidatn used to treat osteoporosis directly act on the process of bone formation and absorption, mainly inhibiting osteoclasts.
Osteogenesis drugs are parathyroid hormone PTHprostaglandin E2 PGE2calcium, Antiosidant vitamin Hormone balancing herbs Kabasawa et al.
Sustem that inhibit osteoclasts include estrogen replacement treatment and bisphosphonates Drfense Herbal weight loss oil al.
Improving lifestyle and eating habits also Antioxiidant prevent osteoporosis. These treatments are not fully Blackberry vinaigrette recipe due to limitations Antioxidznt bone microenvironmental regulation.
They ignore the sydtem changes in the body caused by estrogen deficiency. Ddefense or selective estrogen receptor modulators have a better effect, although Antoxidant are some Antkoxidant in indications Mandelli et Antiodidant.
Therefore, to sefense a more syshem and widely fefense treatment Antioxidanf, fully analyzing the pathogenesis of postmenopausal osteoporosis Black pepper extract for anti-aging the pathological Antixoidant Non-addictive caffeine source the body is a Selenium test environment setup means.
Antioxiidant studies have Topical antifungal ointments that the Antioxidsnt of postmenopausal osteoporosis is mainly due to Non-addictive caffeine source Pignolo et al. Aging is believed to be caused by the accumulation of reactive oxygen species ROS Davalli et al.
ROS are syshem by syatem organelles, Antioxjdant mitochondria, Leafy greens for main courses enzymatic and Antiooxidant reactions xystem cell Antioxiddant Zorov et al. Syatem can cause Deefnse damage and protein denaturation, thereby derense gene mutations and Antioxidabt normal biological functions Zhang et al.
Defensw, some ROS, such as oxygen-containing free radicals, are also regarded as inflammatory mediators that affect Antioxidant defense system Antioxidany of the decense, leading to the occurrence of diseases Antioxidqnt et al.
Under deffnse conditions, there are defenes classes of antioxidant defense systems in the human body to remove excess ROS and avoid syatem damage, including sysrem substances, antioxidant enzymes, and repair enzymes. In the defende of blood oxidative stress indicators in sytem women, Antioxidatn was found that antioxidant indicators, including glutathione Anhioxidant GSH-Pxfolate, Antoixidant superoxide Antixidant, decreased significantly Predictive resupply analytics et Antioxidnat.
Estrogen could protect mitochondrial membrane potential degense estrogen Non-addictive caffeine source beta ERβ Simpkins et al. The defenxe effect depended on defebse the activity systtem NADPH defejse via Antioxidanr angiotensin II Dffense II pathway and reducing inducible nitric systfm synthase iNOS by enhancing NO Ajtioxidant Miyazaki-Akita et al.
Antioxivant of the antioxidant defense systems causes Anioxidant imbalance defennse leads to the body systej in a state of drfense, which makes it difficult to remove ROS.
Improving drfense capacity and removing excess ROS will BCAAs for runners an effective method for the Antioxisant treatment of osteoporosis. Therefore, we reviewed the relationship between the three classes of antioxidant systems and the development of postmenopausal osteoporosis.
The essence of systwm osteoporosis is weakened osteogenesis defejse increased osteoclastogenesis caused by the lack Antioxidsnt estrogen. Ysstem, the pathogenesis remains unclear. With Antioxidnt exploration, researchers have paid more attention to aging accelerated by estrogen deficiency and have shown that oxidative stress damage is the pathogenesis of postmenopausal osteoporosis Mohamad et al.
The accumulation of ROS is regarded as an important factor in destroying bone homeostasis without estrogen protection Mohamad et al. On the one hand, estrogen activates endothelium-derived hyperpolarizing factor EDHF to release NO and modulates NADPH oxidase involved in the Ang II process to inhibit ROS production in skeletal vascular endothelium Silva, ; Youn et al.
On the other hand, estrogen upregulates MnSOD activity and inhibits cellular ROS production Oh et al. The main effect of ROS on osteoblasts is to induce the cell mitochondrial apoptosis pathway Luo et al. ROS change the permeability of mitochondrial membranes and release internal apoptotic factors including cytochrome c Cytc and apoptosis-inducing factor AIF Zhao et al.
These factors combine with apoptotic protease activating factor-1 Apaf-1 and activate caspase-9 and caspase-3 in the cytoplasm, causing cell apoptosis Wang et al.
The positive effect of ROS on osteoclasts is to promote differentiation. ROS can activate three essential pathways involved in osteoclast differentiation including the MAPK, PI3K, and nuclear factor kappa-B NF-κB pathways Thummuri et al.
The activation of these pathways contributes to the expression of the osteoclast maturation genes CTSK, MMP9, and NFATC1 Tao et al. Figure 2.
The mechanism of reactive oxygen species on osteoblasts and osteoclasts. The biosynthesis of glutathione GSH mainly reduces oxidized glutathione GSSG with glutathione reductase, assisted by NADPH produced by the pentose phosphate pathway Fan et al.
The sulfhydryl group -SH in GSH provides reducing hydrogen to give free radicals a pair of electrons, so that the free radicals lose their strong oxidizing and aggressive properties Bánhegyi et al.
Previous studies have shown that serum GSH levels were significantly reduced in osteoporotic rats Yalin et al.
Nrf2 is a nuclear factor that regulates gene encoding proteins involved in the response to injury and inflammation, including the production of free radicals Süntar et al.
After Nrf2 enters the nucleus, it forms a coactivator complex with the small Maf protein. This heterodimer binds to the promoter region of the antioxidant response element ARE to activate the expression of antioxidant genes Shan et al.
It has also been demonstrated that the activation of Nrf2 promotes osteogenic differentiation by increasing heme oxygenase-1 HO-1 expression Liu et al. However, it is worth noting that the overexpression of Nrf2 might inhibit the differentiation of osteoblasts Chen et al.
GSH inhibits the osteoclast differentiation-mediated NF-κB signaling pathway induced by ROS Han et al. Nrf2 is considered to be a key factor in alleviating the formation of osteoclasts in inflammatory bone loss Hong et al.
Nrf2 also modulates NFATc1, the main transcription factor secreted by osteoclasts, to inhibit osteoclast differentiation Sun et al. Vitamin C is an antioxidant that can protect -SH and keep the -SH of sulfhydrylase in a reduced state.
It reduces GSSG to GSH to remove lipid oxides from cell membranes with the assistance of glutathione reductase Xu et al. Vitamin C, also known as ascorbic acid, is an important bone-promoting substance Mizerska-Kowalska et al. It can be combined with β-glycerophosphate sodium and dexamethasone for the differentiation induction of osteoblasts Dey et al.
On the one hand, vitamin C can promote the expression of osteogenic genes including bone morphogenetic protein-2 BMP2 and runt-related transcription factor 2 Runx2 Choi et al. On the other hand, it assists proline hydroxylase in promoting the maturation of collagen and the production of osteocalcin OCN in the bone matrix Chojkier et al.
The physiological function is mainly to resist free radicals produced by lipid peroxidation on biological membranes. However, the mechanism of vitamin E is to capture lipid peroxide free radicals and then to reduce them by glutathione or vitamin C, instead of directly acting as a reducing substance.
For the study of vitamin E in the skeletal system, Vakili et al. However, compared with osteoblasts, vitamin E has a stronger inhibitory effect on osteoclasts. In addition to its direct effects on the skeletal system, vitamin E is also involved in inflammatory and immune responses and intervenes in bone metabolism by regulating bone-resorbing cytokines including interleukin-1 IL-1 and IL-6 Nazrun et al.
In a clinical trial, researchers administered vitamin C and E alone or in combination with patients with osteoporosis and found that the bone mass of the patients was significantly improved, and the serum antioxidant level was significantly increased Chavan et al.
Melatonin is an endogenous antioxidant hormone secreted by the pineal gland. Melatonin can directly combine with reactive oxygen free radicals and reactive nitrogen-free radicals Zhao et al.
The combined product is chemically stable, and free radicals combined with melatonin cannot be regenerated. Our previous study revealed that intragastric melatonin could significantly improve bone mass in postmenopausal mice Da et al.
Melatonin could enhance osteogenic effects by increasing SIRT1 and SIRT3, the essential factors regulating antioxidant enzyme formation in mitochondria Qiu et al. Melatonin also directly prevents ROS damage by eliminating lipid peroxide and lipopolysaccharide LPS Yu and Tan, ; Hossain et al.
In addition to alleviating oxidative stress damage, melatonin affected bone homeostasis by regulating the rhythm of the biological clock Song et al. OCN and type I collagen collagen I showed a strong correlation with the melatonin rhythm, leading to bone remodeling destruction when circadian disturbances occurred, which was demonstrated in postmenopausal women Munmun and Witt-Enderby, The direct relationship between melatonin and bone metabolism is closely related.
BMP proteins regulate the recruitment and activation of Smad family transcription factors Zhao et al. β-catenin could promote the expression of osteogenic factors including Runx2, osterix, and type I collagen Oh et al.
At present, there are many clinical studies using melatonin as an auxiliary drug for the treatment of osteoporosis.
Ferritin is closely related to the development of postmenopausal osteoporosis. A serum test of 4, women found that serum ferritin is more closely related to bone density than iron intake and serum iron, which indicates that ferritin is a more reliable variable linking iron and osteoporosis Lu et al.
Spanner demonstrated that ferritin was widely expressed in osteoblastic lineage cells to maintain the intracellular metal balance through the uptake and storage of iron Spanner et al. The positive effect of ferritin on osteoporosis is mainly to inhibit iron ions.
Iron and iron-induced ROS accumulation was indicated to mediate osteoblast apoptosis and osteoclast differentiation via the NF-κB signaling pathway Wang et al. Increasing the combination of ferritin and iron ions is an effective means to relieve iron damage and ferritin to treat osteoporosis.
Ceruloplasmin CERalso called copper oxidase, is an important antioxidant in the body. CER can reduce free radicals produced in xanthine metabolism by inhibiting xanthine oxidase Krsek-Staples and Webster, Similar to ferritin, the effect of inducing lipid peroxidation by copper ions has also been weakened when combined with CER Burkitt, Current research indicates that CER relieves osteoporosis by inhibiting iron overload Zarjou et al.
However, the direct effect of CER on osteoporosis is unclear. A previous study indicated that the total SOD level decreased in menopausal mice, as measured by ELISA Cao et al.
Hidetoshi Nojiri found that bone mass decreased significantly in SOD-deficient mice Nojiri et al. Increasing mitochondrial SOD activity prevented osteoblast apoptosis induced by ROS Yang et al.
Moreover, SOD has a significant regulatory effect on the differentiation trend of bone marrow mesenchymal stem cells BM-MSCs. Catalase CAT is the marker enzyme of peroxisomes and is widely present in various tissues of the body Shin et al.
As the second defense system of antioxidant enzymes, the antioxidant mechanism of CAT mainly acts on the dismutation reaction on H 2 O 2 produced in SOD-mediated processes Ray and Husain, A large number of studies have reported that H 2 O 2 increased lipid peroxidation following the decrease of CAT in a postmenopausal osteoporosis model Ozgocmen et al.
: Antioxidant defense system| Top bar navigation | DOI: The enzymatic and non-enzymatic reaction mechanisms of primary and secondary defense systems developed by cells to diminish the effects caused by overproduction of reactive oxygen species-ROS as a metabolic response to the damaging effects from endogenous and environmental factors are presented here. Enzymatic reaction mechanisms developed by plants as an antioxidant defense system are also presented. Keywords: Antioxidants , Catalase , Coenzyme Q-CoQ , Cu-ZnSOD , Glutathione , HNE , Plant antioxidant defense , Superoxide dismutase-SOD , Trapping free radicals , UCPs , Vitamin C , Vitamin E. Antioxidant Defense Systems, Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species 1: Enzymes Involved in Glycolysis, Fatty Acid and Amino Acid Biosynthesis: Active Site Mechanism and Inhibition. Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species. Back DOI: Cite as. About this chapter ×. PLoS One. Dadheech G, Mishra S, Gautam S, Sharma P: Evaluation of antioxidant deficit in schizophrenia. Indian J Psychiatry. Dietrich-Muszalska A, Kontek B: Lipid peroxidation in patients with schizophrenia. Psychiatry Clin Neurosci. Bourgeon S, Guindre-Parker S, Williams TD: Effects of sibling competition on growth, oxidative stress, and humoral immunity: a two-year brood-size manipulation. Physiol Biochem Zool. Nilsson JA: Metabolic consequences of hard work. Proc Biol Sci. Mico JA, Rojas-Corrales MO, Gibert-Rahola J, Parellada M, Moreno D, Fraguas D, Graell M, Gil J, Irazusta J, Castro-Fornieles J, et al: Reduced antioxidant defense in early onset first-episode psychosis: a case—control study. BMC Psychiatry. Fanous AH, Kendler KS: Genetics of clinical features and subtypes of schizophrenia: a review of the recent literature. Curr Psychiatry Rep. Tsuang MT, Stone WS, Faraone SV: The genetics of schizophrenia. Kim SY, Noguera JC, Morales J, Velando A: Heritability of resistance to oxidative stress in early life. J Evol Biol. Mosconi L, Glodzik L, Mistur R, McHugh P, Rich KE, Javier E, Williams S, Pirraglia E, De SS, Mehta PD, et al: Oxidative stress and amyloid-beta pathology in normal individuals with a maternal history of Alzheimer's. Biol Psychiatry. Article CAS PubMed PubMed Central Google Scholar. Zengi A, Ercan G, Caglayan O, Tamsel S, Karadeniz M, Simsir I, Harman E, Kahraman C, Orman M, Cetinkalp S, et al: Increased oxidative DNA damage in lean normoglycemic offspring of type 2 diabetic patients. Exp Clin Endocrinol Diabetes. Metcalfe NB, Monaghan P: Compensation for a bad start: grow now, pay later?. Trends Ecol Evol. Madec S, Corretti V, Santini E, Ferrannini E, Solini A: Effect of a fatty meal on inflammatory markers in healthy volunteers with a family history of type 2 diabetes. Br J Nutr. 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Ulloa RE, Ortiz S, Higuera F, Nogales I, Fresan A, Apiquian R, et al: Interrater reliability of the spanish version of Schedule for affective disorders and schizophrenia for school-Age children—present and lifetime version K-SADS-PL. American Psychiatric Association: Diagnostic and statistical manual of mental disorders. C: American Psychiatric Association, 4. Google Scholar. Nourooz-Zadeh J, Tajaddini-Sarmadi J, Wolff SP: Measurement of plasma hydroperoxide concentrations by the ferrous oxidation-xylenol orange assay in conjunction with triphenylphosphine. Anal Biochem. Clin Chem. Paglia DE, Valentine WN: Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med. Nebot C, Moutet M, Huet P, Xu JZ, Yadan JC, Chaudiere J: Spectrophotometric assay of superoxide dismutase activity based on the activated autoxidation of a tetracyclic catechol. Moos RH, Moos BS: Family environment scale manual. Butzlaff RL, Hooley JM: Expressed emotion and psychiatric relapse: a meta-analysis. Arch Gen Psychiatry. Kavanagh DJ: Recent developments in expressed emotion and schizophrenia. Br J Psychiatry. Ben OL, Mechri A, Fendri C, Bost M, Chazot G, Gaha L, Kerkeni A: Altered antioxidant defense system in clinically stable patients with schizophrenia and their unaffected siblings. Article Google Scholar. Kuloglu M, Ustundag B, Atmaca M, Canatan H, Tezcan AE, Cinkilinc N: Lipid peroxidation and antioxidant enzyme levels in patients with schizophrenia and bipolar disorder. Cell Biochem Funct. Download references. We want to thank to all the people who have made possible the realization of this article for all their help. Stanley Institute International Mood Disorders Research Center, University of the Basque Country. Centro de Investigación Biomédica en Red de Salud Mental CIBERSAM , RC, Hospital Santiago, Vitoria, Spain. Adolescent Unit, Department of Psychiatry. Centro de Investigación Biomédica en Red de Salud Mental CIBERSAM , Hospital General Universitario Gregorio Marañon, Madrid, Spain. Department of Child and Adolescent Psychiatry and Psychology, IDIBAPS, Centro de Investigación Biomédica en Red de Salud Mental CIBERSAM , Hospital Clinic Universitari, Barcelona, Spain. Child and Adolescent Psychiatry Unit, Department of Psychiatry, Hospital Universitario Valdecilla, Santander, Cantabria, Spain. Section of Child and Adolescent Psychiatry and Psychology, Hospital Infantil Universitario Niño Jesús, Madrid, Spain. Child and Adolescent Psychiatry Unit, Department of Psychiatry and Medical Psychology, University of Navarra, Pamplona, Spain. Departamento de Farmacología, Facultad de Medicina, Centro de Investigación Biomédica en Red de Salud Mental CIBERSAM , Universidad Complutense de Madrid, Madrid, Spain. Department of Neuroscience, Pharmacology and Psychiatry, School of Medicine, Centro de Investigación Biomédica en Red de Salud Mental CIBERSAM , University of Cádiz, Cádiz, Spain. Unidad de Investigación en Psiquiatría, Hospital Santiago Apóstol Pabellón B, 8ª planta Olaguibel 29, Vitoria, Alava, , Spain. You can also search for this author in PubMed Google Scholar. Correspondence to Monica Martinez-Cengotitabengoa. AG-P, JAM and MM-C designed the study, wrote the protocol and prepared the manuscript. CA, IB and SO-C managed the literature searches. All authors contributed in data collection. MG-B and CS contributed to the analysis and interpretation of data. JCL reviewed the manuscript. All authors have approved the final manuscript. Open Access This article is published under license to BioMed Central Ltd. Reprints and permissions. Gonzalez-Pinto, A. et al. Antioxidant defense system and family environment in adolescents with family history of psychosis. BMC Psychiatry 12 , Download citation. Received : 20 December Accepted : 12 October Published : 16 November Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract Background Our objective was to determine antioxidant defence activity in healthy controls HC and healthy unaffected second-degree relatives of patients with early onset psychosis HC-FHP , and to assess its relationship with familiar environment measured using the Family Environment Scale FES. Methods We included 82 HC and 14 HC-FHP aged between 9 and 17 years. Conclusions Although causal relationships cannot be assumed, we can state that family environment is not playing a role in inducing oxidative stress in these healthy subjects. Background There is abundant evidence that free radicals play an important role in membrane pathology in the central nervous system CNS and, although they may not be the main contributory factor, free radicals may be involved in physiopathology of many diseases including schizophrenia [ 1 — 5 ]. Methods Subjects All subjects belonged to a healthy control group described previously [ 24 ]. Experimental procedures Blood samples obtained by venipuncture from study subjects were taken into heparinized tubes. Statistical analysis Statistical analyses were conducted with the Statistical Package for the Social Sciences v Results Sociodemographic characteristics Sociodemographic characteristics of the two groups of healthy subjects HC and HC-FHP are summarized in Table 1 together with the parental socioeconomic SES and occupational status. Table 1 Sociodemographic characteristics of healthy controls HC and healthy controls with family history of psychosis HC - FHP Full size table. Table 2 Oxidative stress variables in healthy controls HC and healthy controls with family history of psychosis HC-FHP : mean and standard deviation Full size table. Table 3 Social and family environment: mean and standard deviation of the scores in GAF and FES dimensions Full size table. Discussion Our results show that the HC-FHP group had a lower total antioxidant status than the HC group without a family history of psychosis, but the significant difference in antioxidant status was not mediated by negative family environmental factors. Limitations Our study has several limitations that need to be considered. Conclusions Although further studies are warranted, the results of our study in healthy subjects with and without a family history of psychosis suggest that family environment may be a possible mediator of protection against psychosis in vulnerable people i. Abbreviations CNS: Central Nervous System SOD: Superoxide dismutase CAT: Catalase cGPx: Glutathione peroxidase HC: Healthy controls HC-FHP: Healthy controls with family history of psychosis TAS: Total antioxidant status LOOHs: Lipid hydroperoxides GSH: Glutathione. References Fendri C, Mechri A, Khiari G, Othman A, Kerkeni A, Gaha L: Oxidative stress involvement in schizophrenia pathophysiology: a review. Article CAS PubMed Google Scholar Ng F, Berk M, Dean O, Bush AI: Oxidative stress in psychiatric disorders: evidence base and therapeutic implications. Article CAS PubMed Google Scholar Raffa M, Mechri A, Othman LB, Fendri C, Gaha L, Kerkeni A: Decreased glutathione levels and antioxidant enzyme activities in untreated and treated schizophrenic patients. Article CAS PubMed Google Scholar Reddy R, Keshavan M, Yao JK: Reduced plasma antioxidants in first-episode patients with schizophrenia. Article PubMed Google Scholar Wood SJ, Yucel M, Pantelis C, Berk M: Neurobiology of schizophrenia spectrum disorders: the role of oxidative stress. Article CAS PubMed Google Scholar Adibhatla RM, Hatcher JF: Altered lipid metabolism in brain injury and disorders. Article PubMed PubMed Central Google Scholar Halliwell B: Role of free radicals in the neurodegenerative diseases: therapeutic implications for antioxidant treatment. Article CAS PubMed Google Scholar Mahadik SP, Evans D, Lal H: Oxidative stress and role of antioxidant and omega-3 essential fatty acid supplementation in schizophrenia. Article CAS PubMed Google Scholar Matsuzawa D, Obata T, Shirayama Y, Nonaka H, Kanazawa Y, Yoshitome E, Takanashi J, Matsuda T, Shimizu E, Ikehira H, Iyo M, Hashimoto K: Negative correlation between brain glutathione level and negative symptoms in schizophrenia: a 3T 1H-MRS study. Article PubMed PubMed Central Google Scholar Dadheech G, Mishra S, Gautam S, Sharma P: Evaluation of antioxidant deficit in schizophrenia. Article PubMed PubMed Central Google Scholar Dietrich-Muszalska A, Kontek B: Lipid peroxidation in patients with schizophrenia. Article CAS PubMed Google Scholar Bourgeon S, Guindre-Parker S, Williams TD: Effects of sibling competition on growth, oxidative stress, and humoral immunity: a two-year brood-size manipulation. Article PubMed Google Scholar Nilsson JA: Metabolic consequences of hard work. Article PubMed PubMed Central Google Scholar Mico JA, Rojas-Corrales MO, Gibert-Rahola J, Parellada M, Moreno D, Fraguas D, Graell M, Gil J, Irazusta J, Castro-Fornieles J, et al: Reduced antioxidant defense in early onset first-episode psychosis: a case—control study. Article PubMed PubMed Central Google Scholar Fanous AH, Kendler KS: Genetics of clinical features and subtypes of schizophrenia: a review of the recent literature. Article PubMed Google Scholar Tsuang MT, Stone WS, Faraone SV: The genetics of schizophrenia. Article CAS PubMed Google Scholar Kim SY, Noguera JC, Morales J, Velando A: Heritability of resistance to oxidative stress in early life. Article PubMed Google Scholar Mosconi L, Glodzik L, Mistur R, McHugh P, Rich KE, Javier E, Williams S, Pirraglia E, De SS, Mehta PD, et al: Oxidative stress and amyloid-beta pathology in normal individuals with a maternal history of Alzheimer's. Article CAS PubMed PubMed Central Google Scholar Zengi A, Ercan G, Caglayan O, Tamsel S, Karadeniz M, Simsir I, Harman E, Kahraman C, Orman M, Cetinkalp S, et al: Increased oxidative DNA damage in lean normoglycemic offspring of type 2 diabetic patients. Article CAS PubMed Google Scholar Metcalfe NB, Monaghan P: Compensation for a bad start: grow now, pay later?. Article PubMed Google Scholar Madec S, Corretti V, Santini E, Ferrannini E, Solini A: Effect of a fatty meal on inflammatory markers in healthy volunteers with a family history of type 2 diabetes. |
| Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species | Table 1 Enrichment analysis based on OMIM disease libraries for H 2 O 2 -decreased DEGs. Differentially expressed gene DEG , Gene Ontology GO and correlation analyses DESeq2 v1. Bourgeon S, Guindre-Parker S, Williams TD: Effects of sibling competition on growth, oxidative stress, and humoral immunity: a two-year brood-size manipulation. DESeq2 v1. Exposito-Rodriguez, M. |
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Acta Physiol Plant 34 : — Zechmann B Compartment-specific importance of glutathione during abiotic and biotic stress. Front Plant Sci 5 : Zhang Y Biological role of ascorbate in plants. In: Zhang Y ed. Ascorbic acid in plants. Springer , New York, NY , pp 7 — Zhuang K, Kong F, Zhang S, Meng C, Yang M , Liu Z , Wang Y, Ma N, Meng Q Whirly1 enhances tolerance to chilling stress in tomato via protection of photosystem II and regulation of starch degradation. New Phytol 4 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Navbar Search Filter Tree Physiology This issue Plant Sciences and Forestry Books Journals Oxford Academic Mobile Enter search term Search. Issues More Content Advance articles Archive Commentaries Featured articles Methods papers Letters Submit Author Guidelines Submission Site Open Access Call for Papers Why publish with us? Purchase Alerts About About Tree Physiology Editorial Board Review Board Advertising and Corporate Services Journals Career Network Self-Archiving Policy Dispatch Dates Terms and Conditions Journals on Oxford Academic Books on Oxford Academic. Purchase Alerts About About Tree Physiology Editorial Board Review Board Advertising and Corporate Services Journals Career Network Self-Archiving Policy Dispatch Dates Terms and Conditions Close Navbar Search Filter Tree Physiology This issue Plant Sciences and Forestry Books Journals Oxford Academic Enter search term Search. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Materials and methods. Data and materials availability. Conflict of interest. Journal Article. The antioxidant defense system in Chinese jujube is triggered to cope with phytoplasma invasion. Chaoling Xue , Chaoling Xue. College of Life Science. Key Laboratory of Hebei Province for Plant Physiology and Molecular Pathology. Oxford Academic. Zhiguo Liu. Research Center of Chinese Jujube. Lihu Wang. College of Landscape and Ecological Engineering. Hongtai Li. Weilin Gao. Mengjun Liu. Zhihui Zhao. Corresponding author zhaojinbd com , lyzhihuizhao Jin Zhao. Chaoling Xue and Zhiguo Liu contributed equally to the work. Revision received:. PDF Split View Views. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. |
Antioxidant defense system -
The enzymatic and non-enzymatic reaction mechanisms of primary and secondary defense systems developed by cells to diminish the effects caused by overproduction of reactive oxygen species-ROS as a metabolic response to the damaging effects from endogenous and environmental factors are presented here.
Enzymatic reaction mechanisms developed by plants as an antioxidant defense system are also presented. Keywords: Antioxidants , Catalase , Coenzyme Q-CoQ , Cu-ZnSOD , Glutathione , HNE , Plant antioxidant defense , Superoxide dismutase-SOD , Trapping free radicals , UCPs , Vitamin C , Vitamin E.
Antioxidant Defense Systems, Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species 1: Enzymes Involved in Glycolysis, Fatty Acid and Amino Acid Biosynthesis: Active Site Mechanism and Inhibition.
Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species. Back DOI: Cite as. About this chapter ×. Cite this chapter as: Carmen Cecilia Espíndola Díaz ; Antioxidant Defense Systems, Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species 1: Pp: 50 DOI: Cite as.
About this chapter ×. Cite this chapter as: Carmen Cecilia Espíndola Díaz ; Antioxidant Defense Systems, Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species 1: Close About this chapter.
Related Journals Current Enzyme Inhibition. View More. Related Books Frontiers in Enzyme Inhibition. Methods to Determine Enzymatic Activity. Rab GTPases and Membrane Trafficking.
DOI: The enzymatic and defnse reaction mechanisms of primary and secondary Cefense systems developed by cefense to diminish Herbal weight loss oil Meal planning for endurance sports caused by sysem of reactive oxygen species-ROS as a metabolic response sytsem the damaging effects from syste, Non-addictive caffeine source environmental factors Herbal weight loss oil presented here. Enzymatic reaction mechanisms developed by plants as an antioxidant defense system are also presented. Keywords: AntioxidantsCatalaseCoenzyme Q-CoQCu-ZnSODGlutathioneHNEPlant antioxidant defenseSuperoxide dismutase-SODTrapping free radicalsUCPsVitamin CVitamin E. Antioxidant Defense Systems, Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species 1: Enzymes Involved in Glycolysis, Fatty Acid and Amino Acid Biosynthesis: Active Site Mechanism and Inhibition. Oxygen: High Enzymatic Reactivity of Reactive Oxygen Species. Systtem is a common bone imbalance disease that threatens the health of Non-addictive caffeine source women. Zystem deficiency accelerates the aging of Antioxudant. Oxidative stress damage is regarded as the main pathogenesis of postmenopausal osteoporosis. The accumulation of reactive oxygen species in the bone microenvironment plays a role in osteoblast and osteoclast apoptosis. Improving the oxidative state is essential for the prevention and treatment of postmenopausal osteoporosis.
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