Estrogen and Gender Effects on Muscle Damage, Inflammation, and Oxidative Stress

2000 ◽  
Vol 25 (4) ◽  
pp. 274-287 ◽  
Author(s):  
Peter M. Tiidus

Information suggests that there may be gender-based differences in skeletal muscle responses to damaging exercise. Evidence demonstrates that estrogen has strong antioxidant properties and may be an important factor in maintaining postexercise membrane stability and limiting creatine kinase (CK) leakage from damaged muscle in female animals. Research demonstrates effects of estrogen and possible gender differences in other morphological and biochemical indices of postexercise muscle damage and leukocyte invasion. Nevertheless, there are conflicting findings suggesting that in some in vivo exercise models, estrogen administration has limited ability to affect exercise-induced oxidative stress and muscle damage and max cause loss of tissue vitamin C. Gender differences appear to exist in tissue levels of other important antioxidants such as vitamin E and glutathione. More research is needed to fully define the potential for estrogen to influence postexercise muscle damage and the inflammatory response and to determine the mechanisms by which it may operate. Key words: exercise, neutrophils, creatine kinase, vitamin E, vitamin C

1999 ◽  
Vol 24 (3) ◽  
pp. 249-266 ◽  
Author(s):  
Allan H. Goldfarb

Several mechanisms have been forwarded to explain the etiology of exercise-induced muscle damage. Free-radical mediated processes appear to be an important component of the inflammatory mediated response. Free radicals have also been demonstrated to be a contributing factor in the loss of calcium homeostasis within the cell. Therefore, one of the proposed treatments for preventing or reducing the extent of this damage is the intervention of free-radical mediated processes. Antioxidants are agents that typically work to prevent free-radical mediated alterations within cells by quenching free radicals. The traditional dietary antioxidants most commonly investigated to inhibit free-radical damage are vitamin E, vitamin C, and beta carotene. Other nutritional agents have also been noted to posses antioxidant properties. Isoflavonoids and some phytochemicals have been proposed to contain antioxidant properties. This paper briefly reviews some aspects of these agents and their role, either proven or proposed, in the prevention of oxidative stress and muscle damage. Key words: vitamin E, vitamin C, beta carotene, genistein, oxidative stress


1996 ◽  
Vol 315 (2) ◽  
pp. 625-629 ◽  
Author(s):  
Klaus-Dieter ASMUS ◽  
René V. BENSASSON ◽  
Jean-Luc BERNIER ◽  
Raymond HOUSSIN ◽  
Edward J. LAND

Redox reactions of endogenous and exogenous sulphur-containing compounds are involved in protection against oxidative damage arising from the incidence and/or treatment of many diseases, including cancer. We have investigated, via pulse radiolysis, the one-electron oxidation of ergothioneine, a molecule with antioxidant properties which is detected at millimolar concentrations in certain tissues and fluids subject to oxidative stress, including erythrocytes and plasma. The spectrum of the transient species, assigned to the product of one-electron oxidation, observed after reaction of ergothioneine with the oxidizing radicals OH•, N3• and CCl3O2• has a maximum absorption at 520 nm and is very similar to that obtained by oxidation of analogous molecules such as 2-mercaptoimidazole, 1-methyl-2-mercaptoimidazole, S-methyl- and S,N-dimethyl-ergothioneine. In the presence of vitamin C, the oxidized form of ergothioneine is repaired by a rapid reduction (k = 6.3×108 M-1·s-1) producing ascorbyl radicals. This co-operative interaction between ergothionine and ascorbate, similar to that previously observed between vitamin E and ascorbate, may contribute to essential biological redox protection.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 120-121
Author(s):  
Chloey P Guy ◽  
Catherine L Wellman ◽  
David G Riley ◽  
Charles R Long ◽  
Ron D Randel ◽  
...  

Abstract We previously determined that prenatal stress (PNS) differentially affected methylation of DNA from leukocytes of 28-d-old calves. Specifically, COX14 (cytochrome c oxidase (COX) assembly factor) and CKMT1B (mitochondrial creatine kinase U-type) were hypomethylated and COA5 (COX assembly factor 5), COX5A (COX subunit 5A), NRF1 (nuclear respiratory factor 1), and GSST1 (glutathione S-transferase theta-1) were hypermethylated in PNS compared to non-PNS calves (P ≤ 0.05). Our current objective was to test the hypothesis that PNS exhibit impaired mitochondrial function and greater oxidative stress than non-PNS calves. Blood and longissimus dorsi muscle samples were collected from yearling Brahman calves whose mothers were stressed by 2 h transportation at 60, 80, 100, 120, and 140 days of gestation (PNS; 8 bulls, 6 heifers) and non-PNS calves (4 bulls, 6 heifers). Serum was evaluated for the stress hormone, cortisol, and muscle damage marker, creatine kinase; muscle was analyzed for mitochondrial volume density and function by citrate synthase (CS) and COX activities, respectively, concentration of malondialdehyde, a lipid peroxidation marker, and activity of the antioxidant, superoxide dismutase (SOD). Data were analyzed using mixed linear models with treatment and sex as fixed effects. Serum cortisol was numerically higher in PNS than non-PNS calves but was not statistically different. Muscle CS and COX activities relative to protein were greater in PNS than non-PNS calves (P ≤ 0.03), but COX relative to CS activity was similar between groups. Activity of COX was greater in bulls than heifers (P = 0.03), but no other measure was affected by sex. All other measures were unaffected by PNS. Prenatal stress did not affect markers of muscle damage and oxidative stress in yearling Brahman calves at rest but mitochondrial volume density and function were greater in PNS calves. Acute stressors induce oxidative stress, so implications of differences in mitochondria in PNS calves following a stressor should be investigated.


2020 ◽  
Vol 11 (SPL4) ◽  
pp. 2807-2813
Author(s):  
Resmi C R ◽  
Kedari G S R ◽  
Deepa P K

CAD is recognized as a multifactorial disease that is influenced by environmental and genetic factors. This study aimed to evaluate the levels of lipid parameters, oxidative stress and antioxidant markers in subjects with CAD compared to their age & sex matched controls and to analyze the relationship between atherogenic Index and oxidative stress among them 62 clinically proved CAD patients and 62 healthy age and sex matched subjects without CAD were selected for this study. 5 ml of fasting venous blood was collected from all the subjects and investigations such as FPG, lipid profile, oxidative markers Malondialdehyde (MDA), F2 isoprostanes (F2iso) and antioxidants glutathione S-transferase (GST), superoxide dismutase (SOD), vitamin-C, vitamin-E were performed. This study showed that levels of lipid parameters total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-c) and AI were significantly higher whereas high density lipoprotein cholesterol (HDL-c) were significantly low in CAD patients compared to normal controls. Oxidative stress markers MDA and F2 Isoprostanes level were significantly high, whereas enzymatic antioxidants GST and SOD and non-enzymatic antioxidants Vitamin-C and Vitamin-E levels were significantly low in CAD patients. Oxidative stress markers were found to significantly influence the AI. Results of this study showed that oxidative stress markers F2iso and MDA and antioxidants GST, VIT-C and VIT-E are found to influence the atherogenic index significantly.


2020 ◽  
Vol 3 (1) ◽  
pp. 31-44
Author(s):  
Bermansyah ◽  
Gama Satria ◽  
Ahmad Umar

Introduction.Pulmonary contusions can cause a progressive inflammatory response. Activation of TNF-α cytokines and reactive oxygen species (ROS) can cause pulmonary cell death. Antioxidants can have the potential to neutralize ROS. The purpose of this study is to determine the effectiveness of antioxidant administration in maintaining pulmonary cell function in wistar rats that have been induced to experience pulmonary contusions through caspase-3 levels. Methods.This study was an in vivo experimental study conducted on thirty male wistar rats and divided into five groups (n = 6): control, pulmonary contusion + asthaxanthine 5 mg/kgBW, pulmonary contusion + vitamin C and E 50 mg/kgBW, pulmonary contusion + vitamin C and E 100 mg/kgBW, pulmonary contusion + vitamin C and E 200 mg/kgBW. The value of Caspase-3 is evaluated by the IHC. All data analyzes used SPSS 18. Results. Low doses of antioxidants have the potential to reduce pulmonary cell death in wistar rats induced by pulmonary contusions.Conclussion. Vitamin C and E effective to reduce polmonary cell death in pulmonary contusion.Keywords: antioxidants, vitamin C, vitamin E, pulmonary contusions animal model, apoptosis, caspase-3


Author(s):  
Shobha S Pajai ◽  
Apurva P Bezalwar

Introduction: Oxidative stress is a complex event determined genetically and induced by an in- utero stressor. Oxidants are composed of reactive free radicals like Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) which are manifested by several macromolecules of lipid, protein and DNA, causing deleterious effects in several organs. Antioxidant defense mechanism and its ability to be induced by hyperoxia is relatively impaired in preterm neonates. Aim: To study oxidative stress and antioxidants in preterm neonates. Materials and Methods: This study is an observational analytical study, which included preterm babies (25 males and 20 females) delivered vaginally from October 2012 to October 2013. Cord blood was collected in citrate bulbs immediately after vaginal delivery and stored at 4°C until processed. Malondialdehyde (MDA), Nitrates, Vitamin C and Vitamin E, levels were measured in cord blood. Statistical z-test was applied. Results: High levels of oxidative stress biomarkers like MDA and Nitrites along with decreased levels of antioxidants, Vitamin C and Vitamin E in preterm neonates was observed. MDA and Nitrates levels were significantly higher in males (p<0.05) than females. Vitamin C and Vitamin E levels were not significant (p>0.05) in both. Conclusion: This study results may conclude that preterm neonates have more oxidative stress especially in males affecting their life survival.


2011 ◽  
Vol 4 (1) ◽  
pp. 20-26 ◽  
Author(s):  
Ružena Sotníková ◽  
Jana Nedelčevová ◽  
Jana Navarová ◽  
Viera Nosáľová ◽  
Katarína Drábiková ◽  
...  

Protection of the vascular endothelium in experimental situationsOne of the factors proposed as mediators of vascular dysfunction observed in diabetes is the increased generation of reactive oxygen species (ROS). This provides support for the use of antioxidants as early and appropriate pharmacological intervention in the development of late diabetic complications. In streptozotocin (STZ)-induced diabetes in rats we observed endothelial dysfuction manifested by reduced endothelium-dependent response to acetylcholine of the superior mesenteric artery (SMA) and aorta, as well as by increased endothelaemia. Changes in endothelium-dependent relaxation of SMA were induced by injury of the nitric oxide radical (·NO)-signalling pathway since the endothelium-derived hyperpolarising factor (EDHF)-component of relaxation was not impaired by diabetes. The endothelial dysfunction was accompanied by decreased ·NO bioavailabity as a consequence of reduced activity of eNOS rather than its reduced expression. The results obtained using the chemiluminiscence method (CL) argue for increased oxidative stress and increased ROS production. The enzyme NAD(P)H-oxidase problably participates in ROS production in the later phases of diabetes. Oxidative stress was also connected with decreased levels of reduced glutathione (GSH) in the early phase of diabetes. After 10 weeks of diabetes, adaptational mechanisms probably took place because GSH levels were not changed compared to controls. Antioxidant properties of SMe1EC2 foundin vitrowere partly confirmedin vivo.Administration of SMe1EC2 protected endothelial function. It significantly decreased endothelaemia of diabetic rats and improved endothelium-dependent relaxation of arteries, slightly decreased ROS-production and increased bioavailability of ·NO in the aorta. Further studies with higher doses of SMe1EC2 may clarify the mechanism of its endothelium-protective effectin vivo.


2001 ◽  
Vol 354 (3) ◽  
pp. 493-500 ◽  
Author(s):  
Jeremy P. E. SPENCER ◽  
Hagen SCHROETER ◽  
Gunter KUHNLE ◽  
S. Kaila S. SRAI ◽  
Rex M. TYRRELL ◽  
...  

There is considerable current interest in the cytoprotective effects of natural antioxidants against oxidative stress. In particular, epicatechin, a major member of the flavanol family of polyphenols with powerful antioxidant properties in vitro, has been investigated to determine its ability to attenuate oxidative-stress-induced cell damage and to understand the mechanism of its protective action. We have induced oxidative stress in cultured human fibroblasts using hydrogen peroxide and examined the cellular responses in the form of mitochondrial function, cell-membrane damage, annexin-V binding and caspase-3 activation. Since one of the major metabolites of epicatechin in vivo is 3′-O-methyl epicatechin, we have compared its protective effects with that of epicatechin. The results provide the first evidence that 3′-O-methyl epicatechin inhibits cell death induced by hydrogen peroxide and that the mechanism involves suppression of caspase-3 activity as a marker for apoptosis. Furthermore, the protection elicited by 3′-O-methyl epicatechin is not significantly different from that of epicatechin, suggesting that hydrogen-donating antioxidant activity is not the primary mechanism of protection.


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