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Results for “Antioxidant defense”

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At least 19 recordsLinked to original sources

PubMed2003

An imbalance in antioxidant defense affects cellular function: the pathophysiological consequences of a reduction in antioxidant defense in the glutathione peroxidase-1 (Gpx1) knockout mouse.

Aerobic cells are subjected to damaging reactive oxygen species (ROS) as a consequence of oxidative metabolism and/or exposure to environmental toxins. Antioxidants limit this damage, yet peroxidative events occur when oxidant stress increases. This arises due to increased radical formation or decreased antioxidative defenses. The two-step enzymatic antioxidant pathway limits damage to important biomolecules by neutralising superoxides to water. However, an imbalance in this pathway (increased first-step antioxidants relative to second-step antioxidants) has been proposed as etiological in numerous pathologies. This review presents evidence that a shift in favor of hydrogen peroxide and/or lipid peroxides has pathophysiological consequences. The involvement of antioxidant genes in the regulation of redox status, and ultimately cellular homeostasis, is explored in murine transgenic and knockout models. The investigations of Sod1 transgenic cell-lines and mice, as well as Gpx1 knockout mice (both models favor H(2)O(2) accumulation), are presented. Although in most instances accumulation of H(2)O(2) affects cellular function and leads to exacerbated pathology, this is not always the case. This review highlights those instances where, for example, increased Sod1 levels are beneficial, and indicates a role for superoxide radicals in pathogenesis. Studies of Gpx1 knockout mice (an important second-step antioxidant) lead us to conclude that Gpx1 functions as the primary protection against acute oxidative stress, particularly in neuropathological situations such as stroke and cold-induced head trauma, where high levels of ROS occur during reperfusion or in response to injury. In summary, these studies clearly highlight the importance of limiting ROS-induced cellular damage by maintaining a balanced enzymatic antioxidant pathway.

Animals↗

PubMed1998

Antioxidant defense potential of rabbit renal tissues after ESWL: protective effects of antioxidant vitamins.

Antioxidant defense potential, malondialdehyde (MDA) levels, and relative hydroxyl radical (OH.) concentrations were measured in order to establish the effects of extracorporeal shock wave lithotripsy (ESWL) on free radical production and antioxidant defense potential of the rabbit kidney tissues. Electron microscopic examination was also performed to observe ultrastructural changes. The antioxidant defense potential of the ESWL-treated tissues was found to be reduced, and the MDA levels increased as compared with controls. Vitamin (vitamin E plus C combination) pretreatment ameliorated antioxidant defense potential in part, prevented increases in MDA levels in the ESWL-treated tissues, and increased the antioxidant defense potential in the control kidney tissues. After ESWL, a significant amount of OH. radical was measured in the affected tissue. This revealed the source of oxidant stress and peroxidation reactions in the ESWL-treated kidney tissue. Vitamin pretreatment caused significant reduction in the OH. radical concentration. In the electron microscopic investigation, some significant subcellular changes, such as endothelial injury, loss of foot processes, damage of glomerular basal membrane, etc., were observed in the ESWL-treated renal tissue slices. Vitamin pretreatment to a great extent prevented formation of these subcellular changes. Our results suggest that the antioxidant capacity of the kidney tissue was reduced after ESWL treatment and that the tissue was exposed to oxidant stress. Vitamin pretreatment exerted significant protection against the radical damage.

Animals↗

PubMed1998

Impaired antioxidant defense system in the kidney tissues from rabbits treated with cyclosporine. Protective effects of vitamins E and C.

Enzymatic antioxidant defense system and antioxidant defense potential (AOP) were studied in kidney tissue from rabbits treated with cyclosporine (CsA, 25 mg/kg/day), antioxidant vitamins (E, 100 mg/kg/day plus C, 200 mg/ kg/day), and CsA plus antioxidant vitamins, and in kidney tissue from control animals. Although no change was observed in superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) and catalase (CAT) activities were found decreased in kidney tissue exposed to CsA for 10 days compared with control tissue. The level of thiobarbituric acid-reagent substances (TBARS) was higher and antioxidant defense potential (AOP) lower in the CsA-treated group compared with the other groups. Histopathological examination reveals important subcellular damage in the renal tissue from the animals treated with CsA. Antioxidant vitamin therapy caused full improvement in the enzyme activities, TBARS levels and AOP, but the subcellular damage was partly ameliorated in the CsA plus vitamin group. Results suggest that CsA impairs the antioxidant defense system and reduces the antioxidant defense potential in the renal tissue. Antioxidant vitamin treatment protects the tissue in part against toxic effects of the drug.

Animals↗

PubMed1985

Pulmonary antioxidant defense mechanisms.

Intrinsic enzymatic and non-enzymatic pulmonary antioxidant defense mechanisms undoubtedly protect the lung against oxidant-mediated environmental stresses and diseases. In addition, new ways of augmenting pulmonary antioxidant defenses are being developed which can be used to bolster disease-overwhelmed intrinsic lung defense mechanisms. Improved understanding of antioxidant defense mechanisms will increase our knowledge of the causes and suggest rational approaches for treating oxidant-induced lung injury.

Acetylcysteine↗

PubMed2004

Oxidative damage during chagasic cardiomyopathy development: role of mitochondrial oxidant release and inefficient antioxidant defense.

In this study, we evaluated the oxidant status and antioxidant defense capabilities of the heart during the course of Trypanosoma cruzi infection and disease development in a murine model system. Our data show that the extent of protein carbonylation and lipid peroxidation is increased in the heart, but not the skeletal muscle, of infected mice. The level of oxidative injury biomarkers in the myocardium consistently increased with chronic disease severity. The antioxidant defense constituted by catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GSR), and reduced glutathione was increased in murine heart and skeletal tissue in response to the stress of T. cruzi infection. After the initial burst, CAT, GPx, and GSR remained unresponsive to the severity of chronic tissue damage in chagasic hearts. The cardiac level of Mn(2+) superoxide dismutase (MnSOD) was diminished in chagasic mice. Our data suggest that the host responds to acute injuries by activating antioxidant defenses that are of sufficient magnitude to scavenge the reactive oxidants in skeletal tissue. The myocardia of infected mice, however, sustain increased oxidative injuries with disease progression. We surmise that MnSOD deficiencies, resulting in the increased release of mitochondrial free radicals, lead to sustained oxidative stress that exceeds the cardiac antioxidant defense capacity and contribute to persistent oxidative damage in chagasic myocardium.

Animals↗

PubMed2026

The transcriptional regulator CasR controls mycobacterial antioxidant defense and biofilm formation via multiple direct targets.

AIMS: The antioxidant defense system of Mycobacterium tuberculosis is critical for pathogenicity and persistence within macrophages, yet the regulatory networks remain poorly understood. This study aims to elucidate the molecular mechanism by which the transcription factor CasR regulates antioxidant defense in mycobacteria through delineation of the regulatory axis linking CasR activity, target gene expression, and the antioxidant phenotype. METHODS AND RESULTS: Using Mycobacterium smegmatis as a model organism, we demonstrate that overexpression of CasR renders the bacteria significantly susceptible to hydrogen peroxide. Electrophoretic mobility shift assay (EMSA) and β-galactosidase reporter analyses reveal that CasR directly binds and represses the promoter of cyp144, an uncharacterized cytochrome P450-encoding gene. Deletion of casRMsmreduces biofilm formation, consistent with the expected derepression of cyp144Msm, a gene that negatively regulates both biofilm and oxidative stress tolerance. EMSA and β-galactosidase activity assays also demonstrate that CasR negatively regulates antioxidant gene katGI, suggesting that CasR exerts a broader, global regulatory role within the mycobacterial antioxidant defense network. Furthermore, we identify isoleucine 18 as a critical residue for the DNA-binding and regulatory function of CasR. CONCLUSION: This study establishes CasR as a pleiotropic transcriptional regulator that directly controls multiple antioxidant genes, including cyp144 and katGI, in mycobacteria. We report a previously unrecognized role for a cytochrome P450 family member in suppressing bacterial antioxidant capacity, as cyp144 overexpression reduces biofilm formation. These findings provide a valuable reference for further investigation into mycobacterial antioxidant mechanisms and identify CasR and Cyp144 as potential targets for the development of anti-tuberculosis drugs.

Biofilms↗

PubMed2000

Defective antioxidant defense system in patients with a human leptin gene mutation.

Antioxidant defense system prevents the organism from the detrimental effects of free radicals via scavenging or inhibiting their formation. Changes in the antioxidant defense mechanisms and alterations of several essential trace elements in both plasma and various tissues of ob/ob mice have been reported previously. Recent finding of the restoration of the defective antioxidant enzyme activity after leptin treatment in ob/ob mice suggests a putative role of leptin in modulation of antioxidant enzyme activity. Therefore, the aim of this study was to investigate whether antioxidant enzymes and trace elements could also be altered in patients with leptin gene mutation. Seven patients (five men and two women, two of them are homozygous and 5 are heterozygous) with leptin gene mutation and 31 healthy, sex- and age-matched and non-related to the patients (24 male and 9 female), control volunteers were enrolled in the study. Plasma and erythrocyte glutathione peroxidase (GSH-Px) and erythrocyte copper-zinc superoxide dismutase (CuZn-SOD) activities were measured spectrophotometrically. Plasma selenium (Se), manganese (Mn), zinc (Zn), copper (Cu), and iron (Fe) levels were measured by atomic absorption spectrophotometry. Mean Cu and Fe levels in patients were not significantly different than those in controls whereas mean Se, Zn and Mn levels were significantly lower in patients than those of controls (P=0.007, P=0.001, and P=0.001, respectively). Erythrocyte GSH-Px (39%), plasma GSH-Px (24%) and erythrocyte CuZn-SOD activities (32%) were significantly lower than those of the control group (P=0.001, P=0.002, P=0.001, respectively). In conclusion, our results demonstrate that the activity of antioxidant enzymes and plasma levels of Se, Zn and Mn levels were decreased in both homozygous and heterozygous subjects with leptin gene mutation. We suggest that both leptin and trace elements might be involved in the modulation of antioxidant defense system.

Adult↗

PubMed1990

Antioxidant defenses in the ground squirrel Citellus citellus. 1. A comparison with the rat.

The antioxidant defenses of the liver, erythrocytes, blood plasma, and interscapular brown adipose tissue (IBAT) of male ground squirrels were compared with those of male rats kept under identical conditions and fed the same diet. Superoxide dismutase (SOD), ascorbate, vitamin E, catalase, glutathione, and enzymes of glutathione metabolism were measured. In general, antioxidant defenses in erythrocytes were lower in ground squirrels than in rats. The same was true in liver, except that catalase-specific activity was higher. In IBAT, ascorbate, vitamin E, catalase, and glutathione reductase were higher than in rat and more of the SOD activity present was cyanide-insensitive (MnSOD). It is suggested that IBAT in ground squirrels may need a relatively greater antioxidant defense because of its important role in thermogenesis, especially in reawakening from hibernation. No major differences in antioxidant defenses between male and female ground squirrels were observed, except that the SOD activity of IBAT was higher in females.

Adipose Tissue, Brown↗

PubMed2004

A novel cis-element that is responsive to oxidative stress regulates three antioxidant defense genes in rice.

All organisms have defense systems against oxidative stress that include multiple genes of antioxidant defense. These genes are induced by reactive oxygen species under condition of oxidative stress. In this study, we found that a 28-bp motif is conserved on the promoter regions of three antioxidant defense genes in rice (Oryza sativa): cytosolic superoxide dismutase (sodCc1), cytosolic thioredoxin (trxh), and glutaredoxin (grx). We demonstrated that the 28-bp sequence acts as a cis-element responsive to oxidative stress by transient expression assay and designated it as CORE (coordinate regulatory element for antioxidant defense). The CORE was activated by methyl viologen treatment and induced a 3.1-fold increase in expression of the reporter gene, but it did not respond to hydrogen peroxide. The expressions of the sodCc1, trxh, and grx genes were coordinately induced by methyl viologen, suggesting that multiple genes involved in antioxidant defense are controlled by a common regulatory mechanism via CORE. Application of the mitogen-activated protein kinase kinase inhibitor caused the constitutive induction of the sodCc1, trxh, and grx genes and the activation of CORE without methyl viologen treatment. These results indicate that a mitogen-activated protein kinase cascade is involved in the gene regulation mediated by CORE.

Antioxidants↗

PubMed1996

Fish antioxidant defenses--a comparative approach.

There are few comparative studies of vertebrate antioxidant defenses (AD) in the literature. Enzymatic (superoxide dismutase, SOD, and catalase, CAT) and non-enzymatic (alpha-tocopherol, beta-carotene, ubiquinol 10 and blood glutathione) antioxidant defenses were investigated in the liver and blood of 37 fish species, 15 marine species of the southeastern Brazilian coast and 22 freshwater species from the Central Amazon basin. More active marine species displayed in general higher concentrations of SOD and CAT in the liver and blood, compared to those of sedentary or bottom-dwelling species. AD status in marine fish m ay be related to the oxygen consumption of the tissues and of the whole organism, while in freshwater AD may be related to physical and chemical characteristics of the environment rather than to activity level. As thermoconformer organisms, most fish must routinely cope with environmental temperature changes and, consequently, with changes in their metabolic rates. The relatively high antioxidant defense levels that typify fishes, even when compared to endotherms such as birds and mammals, may protect aquatic organisms against the consequences of temperature oscillations.

Adaptation, Physiological↗

PubMed2001

A modified dialyzer with vitamin E and antioxidant defense parameters.

BACKGROUND: Oxidative stress, increased lipid peroxidation, and decreased activity of antioxidant systems may contribute to the accelerated development of atherosclerosis in patients receiving hemodialysis therapy for chronic renal failure. We investigated the influence of vitamin E on antioxidant defense parameters in hemodialysis patients who were using a modified dialyzer. METHODS: In eight hemodialyzed patients, erythrocyte antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPX), plasma total antioxidant capacity (TAC), the concentration of plasma malondialdehyde (MDA), and vitamins A, E, and C were investigated. Each parameter was measured before and after hemodialysis. The study was divided into three periods. Each period lasted three weeks, and during this time, 10 hemodialyses were performed. The first and second periods were carried out using the conventional dialyzer, Terumo CL-S15, but during the second period, patients received vitamin E 400 mg perorally after each hemodialysis. The third period was carried out using a modified dialyzer with vitamin E, Terumo CL-E15. All hemodialyzed patients were treated by erythropoietin and received vitamin C 50 mg/day and pyridoxine 20 mg/day during the entire study. RESULTS: The peroral administration of vitamin E led to a significant increase of serum vitamin E (22%), and no influence on other antioxidant defense parameters was found. The modified dialyzer with vitamin E led to a significant increase of serum vitamin E (33%) and TAC and to the significant decrease of plasma MDA. CONCLUSION: The results of our study suggest that the modified dialyzer with vitamin E provided more effective antioxidant defense than peroral administration of vitamin E in our hemodialysis patients.

Administration, Oral↗

PubMed2003

Cadmium-induced antioxidant defense mechanism in freshwater teleost Oreochromis mossambicus (Tilapia).

Antioxidant defenses consisting of catalase, superoxide dismutase (SOD), xanthine oxidase (XOD), glutathione peroxidase (GPX), and glutathione S-transferase were estimated in liver and kidney of freshwater fish subjected to a sublethal concentration of cadmium chloride (Cd2+), i.e., 5 ppm. The aim of the study was to evaluate the role of antioxidant defenses during cadmium-induced oxidative stress. Significant elevations in liver and kidney of all of the above detoxification enzymes were evident from the 7th day onward, were maintained until the 15th day, and then decreased slightly on the 30th day of exposure to cadmium stress. Between the two tissues studied, liver recorded higher activity for all enzymes except GPX, which was elevated significantly in kidney (82.85%). Both liver and kidney recorded more or less similar increases of SOD (86.61% and 86.32%, respectively), and XOD (86.41% and 84.19%, respectively). The findings indicate that tissue glutathione-dependent enzymes as well as other antioxidant enzymes function in protection against Cd2+ toxicity and that these antioxidants provide a first line of defense against Cd2+ before the induction of any metallothionein synthesis occurs.

Animals↗

PubMed1998

Antioxidant defenses and metabolic depression. The hypothesis of preparation for oxidative stress in land snails.

The roles of enzymatic antioxidant defenses in the natural tolerance of environmental stresses that impose changes in oxygen availability and oxygen consumption on animals is discussed with a particular focus on the biochemistry of estivation and metabolic depression in pulmonate land snails. Despite reduced oxygen consumption and PO2 during estivation, which should also mean reduced production of oxyradicals, the activities of antioxidant enzymes, such as superoxide dismutase and catalase, increased in 30 day-estivating snails. This appears to be an adaptation that allows the snails to deal with oxidative stress that takes place during arousal when PO2 and oxygen consumption rise rapidly. Indeed, oxidative stress was indicated by increased levels of lipid peroxidation damage products accumulating in hepatopancreas within minutes after arousal was initiated. The various metabolic sites responsible for free radical generation during arousal are still unknown but it seems unlikely that the enzyme xanthine oxidase plays any substantial role in this despite being implicated in oxidative stress in mammalian models of ischemia/reperfusion. We propose that the activation of antioxidant defenses in the organs of Otala lactea during estivation is a preparative mechanism against oxidative stress during arousal. Increased activities of antioxidant enzymes have also observed under other stress situations in which the actual production of oxyradicals should decrease. For example, antioxidant defenses are enhanced during anoxia exposure in garter snakes Thamnophis sirtalis parietalis (10 h at 5 degrees C) and leopard frogs Rana pipiens (30 h at 5 degrees C) and during freezing exposure (an ischemic condition due to plasma freezing) in T. sirtalis parietalis and wood frogs Rana sylvatica. It seems that enhancement of antioxidant enzymes during either anoxia or freezing is used as a preparatory mechanism to deal with a physiological oxidative stress that occurs rapidly within the early minutes of recovery during reoxygenation or thawing. Thus, a wide range of stress tolerant animals display coordinated changes in antioxidant defenses that allow them to deal with oxidative stress that occurs as part of natural cycles of stress/recovery that alter oxygen levels in tissues. The molecular mechanisms that trigger and regulate changes in antioxidant enzyme activities in these species are still unknown but could prove to have key relevance for the development of new intervention strategies in the treatment of cardiovascular ischemia/reperfusion injuries in humans.

Animals↗

PubMed1999

Higher levels of antioxidant defenses in enalapril-treated versus non-enalapril-treated hemodialysis patients.

We previously reported chronic treatment with angiotensin-converting enzyme inhibitors (ACEis) increases antioxidant defenses in mice. In the present study, however, we examined various antioxidant defenses in chronic hemodialysis (HD) patients either treated with enalapril (10 mg/d) for at least 6 months (+ACEi; n = 11) or untreated (-ACEi; n = 11). The relationship between antioxidant status and HD was investigated by determining oxidative stress markers and antioxidant defenses in a group of chronic HD patients (n = 33) and a group of age-matched controls (n = 29). The effect of a single HD session on those parameters was also evaluated. Before an HD session (pre-HD), HD patients had significantly lower levels of red blood cell (RBC) glutathione (GSH), selenium-dependent glutathione peroxidase activity (RBC-Se-GPx), plasma ubiquinol-10, and alpha-tocopherol than controls. In a randomly selected group of patients (n = 19), a single HD session caused an additional decrease in RBC-GSH and plasma ubiquinol-10 levels. Plasma thiobarbituric acid reactive substance (TBARS) levels were significantly greater in pre-HD patients than controls. Post-HD plasma TBARS levels were similar to control values. The cohort of +ACEi HD patients had greater pre-HD RBC-GSH content, RBC-Se-GPx activity, and plasma beta-carotene concentrations than -ACEi patients (RBC-GSH: +ACEi, 3.1 +/- 0.9 micromol/mL packed RBCs [PRBCs]; -ACEi, 1.2 +/- 0.3 micromol/mL PRBCs [P < 0.05 v +ACEi]; RBC-Se-GPx: +ACEi, 5.8 +/- 0.7 U/mL PRBCs; -ACEi, 4.3 +/- 0.2 U/mL PRBCs [P < 0.05 v +ACEi]; plasma beta-carotene: +ACEi, 0.54 +/- 0.16 micromol/L plasma; -ACEi, 0.19 +/- 0.05 micromol/L plasma [P < 0.05 v +ACEi]). Results show profound alterations in the circulating antioxidant systems of chronic HD patients and that additional oxidative stress occurs during the HD procedure. In addition, in +ACEi HD patients, the levels of several antioxidant defenses are greater than in those in -ACEi HD patients.

Adult↗

PubMed2001

Effects of multinutrient supplementation on antioxidant defense systems in healthy human beings.

Oxidative damage involved in the pathogenesis of many diseases, such as cardiovascular disease, cancer and diabetics. The antioxidant defense system plays an important role in protecting body from oxidative damage. Numerous studies have been shown that a single vitamin or mineral supplementation has the beneficial effect on the antioxidant defense system. However, the overall combined effect of multinutrient supplementation on antioxidant defense system remains to be clarified. In the present double blind, placebo-controlled study, the antioxidative defense system was measured in 34 healthy subjects before and after multinutrient supplementation. Plasma vitamin C, E and beta-carotene, erythrocyte vitamin E, as well as whole blood selenium all showed increase at 5 weeks of supplementation. The activities of catalase (CAT) and glutathione peroxidase (GPX), but not superoxide dismutase (SOD), as well as GSH level were significantly increased at 16 weeks of supplementation. Moreover, the resistance of erythrocytes to 2,2'-Azobis(2-amidinopropane) dihydrochloride (AAPH)-induced oxidation was elevated at 5 weeks after supplementation. These results clearly demonstrated that short-term supplementation (16 weeks) with multinutrient could markedly improve antioxidative vitamin status and enzymatic activities. These improvements also led to the reduction of RBC susceptibility to free radial peroxidation.

Journal Article↗

PubMed1999

Antioxidant defenses in the TNF-treated MCF-7 cells: selective increase in MnSOD.

Oxidative stress has been implicated in the mechanism of tumor necrosis factor-alpha (TNF)-induced apoptosis, raising a question about the status of antioxidant defenses in TNF-sensitive cells. Antioxidant defenses were examined in MCF-7 cells after treatment with TNF. Cell morphology and DNA fragmentation assays were used to confirm increased apoptosis as a result of TNF treatment. The expression and activity of antioxidant defenses were assessed using Northern blot hybridization analyses and biochemical assays, respectively. Five- and ten-fold increases in manganese superoxide dismutase (MnSOD) mRNA were measured after one and five days of TNF treatment, respectively. The expression of copper,zinc superoxide dismutase, catalase or thioredoxin was not altered. An approximate five-fold increase in MnSOD activity followed the change in gene expression, but no difference in the activity of catalase or glutathione peroxidase was seen. Thus, increased MnSOD activity was not accompanied by an increase in other antioxidant defenses and in particular, H2O2-scavenging enzymes. MnSOD has previously been shown to afford protection against TNF-mediated cytotoxicity. The observed lack of increased peroxidase activity is consistent with mitochondrially-generated superoxide anion radical contributing to the mechanism of TNF-induced apoptosis.

Adenocarcinoma↗

PubMed1996

Liver endogenous antioxidant defenses in mice fed AIN-76A diet and infected with murine AIDS.

The effects of murine AIDS infection on endogenous antioxidant defenses in mice fed the AIN-76A liquid diet were investigated. C57BL/6 female mice were divided into 2 groups: one group was injected interperitoneally with LP-BM5 murine retrovirus (MAIDS) stock, and the other group served as the non-infected control. Two weeks after the infection, the mice were killed and livers were excised for biochemical analysis of the antioxidant defenses. Liver reduced glutathione (GSH) levels and activities of both cytosolic superoxide dismutase (SOD) and mitochondrial SOD were significantly depressed by MAIDS infection. Activities of glutathione reductase (GR) selenium (Se)-dependent glutathione peroxidase (GPx), catalase and glutathione-S-transferase (GST) toward 1-chloro-2,4-dinitrobenzene (CDNB) were not affected by MAIDS infection. A previous study by this laboratory using the Lieber-DeCarli (L-D) all purpose liquid diet caused a decline in total SOD activity and GPx activity, but not GSH levels. The results suggest that MAIDS infection depresses liver antioxidant defenses; however, MAIDS infection of mice fed the AID-76A liquid diet depresses different liver antioxidant defense parameters when compared to those of the mice fed the L-D all purpose liquid diet.

Animals↗

PubMed1992

Effect of aging on enzymatic antioxidant defenses in rat liver mitochondria.

Antioxidant defenses within liver mitochondria are pivotal in preventing liver damage from oxidative toxicants. In this study we determined the activities of glutathione peroxidase (GPO), superoxide dismutase (SOD) and glutathione reductase (GRD) in mitochondria from livers of variously aged Fischer 344 rats. A mixed pattern of age-associated alterations in mitochondrial antioxidant activities was observed. In male rats, GRD activity decreased in old age, whereas GPO and SOD activities increased. In female rats, GPO activity decreased with age, but SOD activity increased and GRD activity was unchanged. Age-associated decreases in antioxidant protection from mitochondrial enzymes appeared to be counterbalanced by increases in protection from other enzymes.

Aging↗