Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superoxide dismutase is well known to act as an effective antioxidant enzyme against cellular damage caused by oxidative stresses including ischemia/reperfusion-induced cerebral injury. However, it is still controversial whether or not the activity of endogenous superoxide dismutase changes during cerebral ischemia and reperfusion. In order to elucidate this phenomenon, we assayed the superoxide dismutase activity in the cerebral tissues of gerbils using the chemiluminescence method with a Cypridina luciferin analog. This method was demonstrated to be a sensitive and specific assay for the enzymatic activity of superoxide dismutase in cerebral tissues, which was not subject to interference from proteins or ascorbate. After 3 h of focal and global ischemia, there were no changes in the cerebral tissue superoxide dismutase activities. After 24 h of reperfusion following 1 h of ischemia, the superoxide dismutase activity decreased only approx 20%, whereas the adenylate kinase activities, measured in the same cerebral tissues as those used for superoxide dismutase assay, started to decline 1 h after reperfusion commenced and were approx 50% of the control levels after 24 h. These results show that almost all the activity of endogenous superoxide dismutase is maintained and does not decrease significantly as a result of ischemia/reperfusion-induced cerebral injury.
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PMID:The superoxide dismutase activities of cerebral tissues, assayed by the chemiluminescence method, in the gerbil focal ischemia/reperfusion and global ischemia models. 836 36

Superoxide dismutase (SOD) may not only perform a housekeeping role in filarial worms but also assist in defense against oxidants generated by host immune cells. Both Dirofilaria and Onchocerca adult filariae and microfilariae contain relatively high activities of the antioxidant enzyme SOD; adult Dirofilaria worms also secrete SOD in vitro. In addition, superoxide radicals are relatively impotent against Dirofilaria and Onchocerca microfilariae in vitro. In assessing the role of SOD, we determined the anatomic localization of SOD in D. immitis adult worms by immunolocalization at the light-microscopic level. We found that anti-D. immitis SOD did not stain parasite tissues homogeneously, in support of the hypothesis that SOD does not have only a housekeeping role and that the pattern of staining may suggest another role(s) for SOD.
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PMID:Immunolocalization of superoxide dismutase in Dirofilaria immitis adult worms. 843 99

The antioxidant activity of vitamin A against lipid peroxidation induced by doxorubicin in rat tissues in vivo was investigated. A single ip injection of doxorubicin (30 mg/kg body wt) markedly raised the level of peroxidated lipids measured as TBARS and conjugated dienes in heart and brain membrane preparations. Other tissues, such as retina and liver, did not show any increase of lipid peroxides over control values. Pretreatment of rats with two daily subcutaneous injections of retinol palmitate (0.25 g/kg body wt), for 2 days, before injecting doxorubicin, inhibited peroxidation of heart and brain membrane lipids. The antioxidant action of vitamin A does not appear to be mediated by enhancement of antioxidant enzyme activities committed to detoxify oxygen radicals. Superoxide dismutase and catalase, measured in heart and brain cytosol, were not affected by the vitamin A treatment. On the contrary, a slight increase of catalase activity was observed in heart and brain cytosol from rats that had been treated with doxorubicin. Excess vitamin A may be localized in membranes. Appreciable increase of retinyl esters and retinol was measured in membrane preparations from rats that had been treated with vitamin A, with respect to control animals. Brain and heart membrane preparations from rats receiving vitamin A, assayed in vitro in the presence of an Fe3+ ascorbate induction system, showed a delay at the beginning of the lipid peroxidation and generated lesser amounts of TBARS, with respect to membranes from control rats. Thus, the increase of vitamin A within cell membranes results in an increased resistance of membrane lipids to peroxidation, both endogenously produced and induced in vitro. These results may be consistent with the hypothesis that vitamin A may act as a physiological antioxidant in cell membranes where it is localized.
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PMID:Vitamin A inhibits doxorubicin-induced membrane lipid peroxidation in rat tissues in vivo. 847 Aug 86

We investigated the effects of chronic volume overload in the absence or presence of vitamin E supplements on the cardiac function and contractility, cardiac malondialdehyde (MDA)--a lipid peroxidation product--cardiac antioxidant enzyme activity and antioxidant reserve in canine model. The dogs were divided into three groups of seven dogs each: group I, control; group II, mitral regurgitation (MR) of 4 months duration; and group III, MR of 4 months duration receiving vitamin E (40 U/kg/daily) orally. MR was created by detaching two or more chordae tendinae to raise left atrial pressure to 2.5 to three times normal. MR produced a decrease in the index of myocardial contractility with little change in myocardial function. Decrease in myocardial (left and right ventricles) contractility was associated with an increase in cardiac MDA, and a decrease in cardiac antioxidant reserve and antioxidant enzyme activity. Prevention of volume overload-induced decrease in myocardial contractility by vitamin E was associated with a decrease in cardiac MDA and an increase in cardiac antioxidant reserve and glutathione peroxidase activity towards control levels. Superoxide dismutase and catalase activity remained depressed in vitamin E-treated group. The results indicate that chronic volume overload decreases the contractility of both right and left ventricles and is associated with oxidative stress in both ventricles. These results support the hypothesis that oxygen free radicals are involved in the chronic volume overload-induced cardiac depression.
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PMID:Oxidative stress as a mechanism of cardiac failure in chronic volume overload in canine model. 872 69

We investigated the effects of aging and/or swimming training on the antioxidant enzyme system in diaphragm of mice. Young (2 months old) and old (26 months old) male mice were swimming-trained for 6 weeks (1 h/day, 5 days/week). Cu,Zn-Superoxide dismutase (Cu,Zn-SOD) activity was significantly upregulated with aging, and swimming training definitely enhanced the activity only in young mice. Neither aging nor swimming training had overt effect on Mn-SOD activity. Glutathione peroxidase activity in young mice was significantly increased after training, but not in old mice. Both of immunoreactive Cu,Zn-SOD and Mn-SOD were significantly increased with aging but were unaffected by swimming training. Consequently, physical training significantly enhanced the specific activity of Cu,Zn-SOD in young mice, but not in old mice. Meanwhile, swimming training significantly increased xanthine oxidase activity in both age groups, the extent of the increase being greater in old mice than in young mice. We concluded that the antioxidant enzyme system in mouse diaphragm trends to be upregulated with aging, but that swimming training improved the system only in young mouse diaphragm.
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PMID:Effects of aging and/or training on antioxidant enzyme system in diaphragm of mice. 893 Nov 79

Nitric oxide mediates esophageal peristalsis and lower esophageal sphincter (LES) relaxation. Superoxide produced with inflammation inactivates nitric oxide. Superoxide is cleared in biological systems by superoxide dismutase. We tested the hypothesis that superoxide and the superoxide scavenging system modulate LES function. Transverse strips of muscle from the opossum LES relaxed when stimulated by an electrical field. Diethyldithiocarbamite was used to inhibit copper/zinc superoxide dismutase. Xanthine and xanthine oxidase were used to generate superoxide. Xanthine with xanthine oxidase or diethyldithiocarbamite alone had no effect on the LES. However, xanthine/xanthine oxidase and diethyldithiocarbamite reduced LES relaxation 34.1% and increased its resting tone 71.2%. Superoxide dismutase did not affect LES function, but protected the tissue from the effects of diethyldithiocarbamite and xanthine/xanthine oxidase. These studies are consistent with the hypothesis that superoxide acts by inactivating nitric oxide and suggest that these antioxidant enzyme systems may play a role in the maintenance of LES function.
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PMID:Effects of oxygen radicals and radical scavenging on opossum lower esophageal sphincter. 907 44

We compared the susceptibility to oxidized LDL cytotoxicity of primary human umbilical vein endothelial cells (HUVEC) and EA.hy 926 cells. EA.hy 926 endothelial cells were more susceptible than HUVEC. To determine the basis of this difference, we evaluated the enzymatic antioxidant machinery in the two cell types. The antioxidant enzyme activities of superoxide dismutase, catalase and glutathione peroxidase were significantly lower in EA.hy cells than in HUVEC: 54%, 71% and 8% of the HUVEC enzyme activities respectively. Pre-incubation of the EA.hy 926 endothelial cells with glutathione peroxidase (100 IU/ml) inhibited the cytotoxic effect of oxidized LDL. Superoxide dismutase (300 or 600 IU/ml) and catalase (300 or 600 IU/ml) had no effect. Compared to HUVEC, the higher susceptibility of EA.hy 926 cells to oxidized LDL induced injury may be associated with lower antioxidant defences, in particular with lower glutathione peroxidase activity which is known to eliminate lipid hydroperoxides and thereby to prevent the formation of damaging peroxyl radical intermediates.
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PMID:Comparison of oxidized low-density lipoprotein toxicity on EA.hy 926 cells and human vein endothelial cells: influence of antioxidant systems. 911 4

Catalase, glutathione peroxidase and superoxide dismutase enzymes were determined after administering dexamethasone. Catalase increased its activity over six times (0.388 U/mg DNA) the normal rate, while glutathione peroxidase caused 3 times an increase one hour after dexamethasone injection. Superoxide dismutase increased gradually during the 3 hour treatment. The antioxidant enzyme activities decreased to basal values in the presence of protein synthesis (Cycloheximide) and RNA synthesis (Actinomycin D) inhibitors. The current report demonstrates that the increase of antioxidant enzymes is due to an enzymatic induction mechanism, and not due to an activation process.
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PMID:Induction of antioxidant enzymes by dexamethasone in the adult rat lung. 918 Mar 60

The goal of this study was to examine whether chronic administration of propranolol offers protection against ischemia-reperfusion injury and whether it induces any change in the myocardial endogenous antioxidant enzyme activities and their gene expression. Rats were treated with propranolol (10 mg/kg/day, i.p.) for either 6 or 18 days. Forty-eight h after the last propranolol injection, isolated hearts were subjected to 60 min of global ischemia and 40 min of reperfusion. Resting tension in the control and treated groups after ischemia was 385+/-30 and 150+/-15%; and upon reperfusion was 140+/-11 and 49+/-6%, respectively, as compared to the pre-ischemic values. Recovery of the contractile function in globally ischemic hearts upon reperfusion was about 35% in the treated group as compared to about 16% in the control group at 10 and 20 min. A positive response to catecholamine was observed in hearts from propranolol group (C, 3.41+/-0.36; epi, 6.03+/-0.47 g/g) and was comparable to control hearts (C, 3.55+/-0.31; epi, 6.48+/-0.42 g/g). Myocardial antioxidants, catalase and glutathione peroxidase enzyme activities, in the treated group, prior to ischemia-reperfusion were increased by 67+/-9 and 45+/-11%, respectively, over those in controls. Superoxide dismutase activity did not show any change. The mRNA expression for the three antioxidant enzymes did not change in the hearts of the treated group as compared to control. Lipid peroxidation, both before and after the ischemia-reperfusion episode, was significantly reduced in the propranolol-treated hearts compared to the control group. Hearts studied at the end of reperfusion showed no difference in enzyme activities between treated and control groups. These data show that propranolol treatment of the animals protects against ischemia-reperfusion injury in isolated hearts in the absence of beta-blockade. Increased endogenous antioxidant enzyme activities due to propranolol treatment may have a role in this protection.
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PMID:Chronic treatment with propranolol induces antioxidant changes and protects against ischemia-reperfusion injury. 944 39

1. At premature birth, man and animals are exposed to relatively high oxygen levels, compared with intra-uterine conditions, at a time when their antioxidant enzyme (AOE) system is still immature. Using the chick embryo as a study model, we investigated changes in the AOE system in response to hyperoxia applied at different time points during the incubation period. Relations between hyperoxia and AOE activity were studied in selected organs (brain, heart, liver, intestine and lungs) of developing chick embryos (during the second half of the incubation period). 2. Incubated White Leghorn eggs were divided into four groups: control (n = 100) and three test groups exposed for 48 h to 60 % O2 on day 10 (test group 1, n = 80), day 14 (test group 2, n = 60) and day 18 (test group 3, n = 30). Superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) enzyme activities were measured in homogenates of the brain, heart, liver, intestine and lungs. 3. Exposure to hyperoxia at different time points during incubation resulted in a 2- to 10-fold increase in SOD activity in all organs except the brain. Catalase and GPx enzyme activities were only induced in test group 1, 48 h after initiation of hyperoxia. 4. In the developing chick embryo, hyperoxia can produce a temporary induction of AOE activity, which is dependent on the AOE, organ, incubation time and time point of exposure.
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PMID:Induction of antioxidant enzyme activity by hyperoxia (60 % O2) in the developing chick embryo. 954 1


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