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)

Glutamate (Glu) is a major excitatory amino acid neurotransmitter in the mammalian brain. Under Certain Circumstances Glu can also exert toxic effects on neuronal Cells. To unravel the biochemical mechanisms of Glu-induced acute neuronal injury, Glu 1 mumol/1 mul was microinjected into cerebral Cortex, striatum and hippocampus of adult rats and oxidative stress and antioxidant parameters were evaluated. The results show that the rate of lipid peroxidation was significantly increased in the above brain regions following Glu administration suggesting neuronal membrane damage and also the total and free sulfhydryl groups were significantly depleted, indicating altered red-ox status of the cells. There was also alteration in the activity of antioxidant enzyme catalase in cerebral cortex. Some of the above Glu-induced effects were reversed or modified by NMDA receptor antagonist MK-801.
Biochem Mol Biol Int 1997 Dec
PMID:Single microinjection of L-glutamate induces oxidative stress in discrete regions of rat brain. 944 17

We have recently developed a porcine model with naturally occurring hypertrophic cardiomyopathy (HCM). Similar to humans, occluded intramural coronary artery and damaged mitochondria are frequently observed in these animals in which the disease is thought to be associated with the local ischemia of myocardium. In view of antioxidant functions involved in the ischemic injury, we measured the expression of endogenous antioxidant enzymes in the tissues with and without HCM. The results showed a significant increase of Cu,Zn-superoxide dismutase (SOD), but not Mn-SOD, and decrease of catalase (CAT) activities in the various areas of HCM hearts. It was demonstrated that SOD/CAT ratios in the HCM hearts were significantly higher than those in normals and were found to be dramatically correlated with the severity of cardiac hypertrophy. The altered SOD/CAT ratio was also consistent with increase in lipid damage. We hypothesize that the elevated SOD combined with an inadequate amount of H2O2 scavenging enzyme may lead HCM heart at oxidative stress risk. However, the pathogenic role of imbalanced antioxidant enzyme needs to be further explored.
Biochem Mol Biol Int 1997 Dec
PMID:Alteration of endogenous antioxidant enzymes in naturally occurring hypertrophic cardiomyopathy. 944 21

Dietary calorie restriction extends both mean and maximum life span and retards age-related diseases, including eye lens cataract in Emory mice. The beneficial effects of calorie restriction have been hypothesized to reflect enhanced tissue antioxidant capacity. As a test of this hypothesis, we reared male and female Emory mice on control (C) or 40% calorie-restricted (R) diets. We then determined activities of total superoxide dismutase (T-SOD), Cu/Zn-SOD, Mn-SOD, glutathione peroxidase (GPx), glutathione reductase (GR) and catalase (CAT) in eye lens, liver and kidney of young (4.5 or 6 months), mature (11 or 12 months) and old (22 months) animals. Effects of diet, age and sex were evaluated by multi-factor ANOVA. Only kidney GR activities (mean +/- S.E.M.) were significantly enhanced with the R diet (R, 61 +/- 2 vs. C, 54 +/- 3 U/mg protein; P = 0.03). More frequently, we noted reduced antioxidant enzyme activity in R as compared with C animals, including reduced activities of T-SOD in lens, liver and kidney, Cu/Zn-SOD in liver and kidney, liver Mn-SOD and liver CAT (P < 0.05). Effects of age on antioxidant enzyme activity in C mice included age-dependent decreases in lens and kidney CAT and in liver Mn-SOD. There was also an age-dependent increases in liver and kidney Cu/Zn-SOD and liver GR. None of these age-dependent alterations in antioxidant enzyme function were attenuated in tissues of mice fed the R diet. Values for liver CAT were significantly lower in females than in males (P = 0.05). These results indicate that antioxidant enzyme activities in Emory mouse tissues are influenced by diet, age and sex. However, it is unlikely that increased lifespan and attenuation of cataract (and perhaps other age-dependent debilities), which are associated with the R diet in the Emory mouse, are due to enhanced antioxidant enzyme capabilities.
Mech Ageing Dev 1997 Dec 30
PMID:Antioxidant enzyme activities in lens, liver and kidney of calorie restricted Emory mice. 948 91

Chick embryos were treated with different concentrations (25 and 75 mumoles/kg egg wt.) of zinc on the 14th day of embryonic development. The levels of thiobarbuturic acid reacting substances (TBARS), glutathione (GSH) and activity levels of antioxidant enzymes such as glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase were measured in both hepatic and brain tissues after different time intervals (24 h, 72 h and 120 h) of zinc exposure. Increased levels of TBARS were observed after 24 h of zinc treatment and thereafter (72 h and 120 h) the levels were decreased in both the tissues. Significant induction was observed in antioxidant enzyme activities in both the tissues after 24 h and 72 h when compared to 120 h. However, the GSH levels were increased at 24 h and 72 h and thereafter decreased in both the tissues at 120 h. The elevated levels of antioxidant enzymes at 24 h and 72 h may be responsible for the reduction of TBARS at 72 h and 120 h in developing chick embryos.
J Enzyme Inhib 1997 Dec
PMID:Effect of zinc on lipid peroxidation and antioxidant enzymes in hepatic and brain tissues of chick embryos. 950 49

We evaluated oxidative stress associated with a model of experimental epilepsy. Male Wistar rats were injected i.p. with 150 mg/kg convulsant 3-mercaptopropionic acid and decapitated in two stages: during seizures or in the post-seizure period. Spontaneous chemiluminescence, levels of thiobarbituric acid reactive substances, total antioxidant capacity and antioxidant enzyme activities were measured in cerebellum, hippocampus, cerebral cortex and striatum. In animals killed at seizure, increases of 42% and 90% were observed in spontaneous chemiluminescence of cerebellum and cerebral cortex homogenates, respectively, accompanied by a 25% increase in cerebral cortex levels of thiobarbituric acid reactive substances. In the post-seizure stage, emission completely returned to control levels in cerebral cortex and partly in cerebellum, thus showing oxidative stress reversibility in time. Hippocampus and striatum seemed less vulnerable areas to oxidative damage. A 30% decrease in glutathione peroxidase activity was only observed in cerebral cortex during seizures, while catalase and superoxide dismutase remained unchanged in all four areas during either stage. Likewise, total antioxidant capacity was unaffected in any of the studied areas. It is suggested that oxidative stress in this model of epilepsy arises from an increase in oxidant species rather than from depletion of antioxidant defences.
Neurochem Res 1998 Dec
PMID:Regional vulnerability to oxidative stress in a model of experimental epilepsy. 982 Nov 50

Using reaggregating rat brain cell cultures at two different stages of differentiation, we examined the biochemical effects of a 10-day treatment with nanomolar concentrations of methylmercuric chloride (monomethylmercury), in the presence or absence of promoters of hydroxyl radical formation (10 microM copper sulphate plus 100 microM ascorbate). A decrease in total protein content accounted for the general cytotoxicity of these compounds, whereas selective effects were assessed by determining the activities of cell type-specific enzymes. Methylmercury, up to 100 nM, as well as the copper ascorbate mixture, when applied separately, induced no general cytotoxicity, and only slight effects on neuronal parameters. However, when applying 100 nM methylmercury and the copper-ascorbate mixture together, a drastic decrease in neuronal and glial parameters was found. Under these conditions, the content of reactive oxygen species, assessed by 2',7'-dichlorofluorescin oxidation, increased greatly, while the activities of antioxidant enzymes decreased. In the presence of copper and ascorbate, differentiated cultures appeared more resistant than immature ones to low methylmercury concentrations (1-10 mM), but did undergo similar changes in both cell type-specific and antioxidant enzyme activities at 100 nM methylmercury. These results suggest that in prooxidant conditions low doses of mercury can become much more deleterious for the central nervous system.
Acta Neuropathol 1998 Dec
PMID:Increased vulnerability of neurones and glial cells to low concentrations of methylmercury in a prooxidant situation. 984 92

Chimeric epidermal reconstructs made with Negroid melanocytes and Caucasoid keratinocytes (or vice versa) were studied before and after UVB irradiation to understand the respective roles of these cells in tanning and photoprotection, especially lipoperoxidation and enzymatic defences against free radicals. Using this approach, we have confirmed overall the theory of the epidermal melanin unit. We have also shown that melanocytes of poorly tanning Caucasoids, which have a comparatively higher content of unsaturated fatty acids in their cell membrane, are more prone to the peroxidative effects of UV light, and that keratinocytes participate in photoprotection via phototype-dependent antioxidant enzyme activities, especially for catalase.
J Invest Dermatol 1998 Dec
PMID:Chimeric human epidermal reconstructs to study the role of melanocytes and keratinocytes in pigmentation and photoprotection. 985 24

The effect of methotrexate (MTX) and leucovorin (LCV) on pentose cycle enzymes and the activity of enzymes involved in enzyme defence mechanisms against ROS in HeLa cells, were studied. The effect of MTX was also investigated on the cellular levels of glutathione. MTX inhibited the activity of glucose-6-phosphate and 6-phosphogluconate dehydrogenases. The activities of glutathione reductase and gamma-glutamylcysteine synthetase were also inhibited by the drug. No effect was observed on the activities of catalase, superoxide dismutase or transketolase. LCV had no effect on any of the enzymes studied. MTX decreased the cellular levels of glutathione (70 per cent), while the presence of LCV and glutamine did not interfere with the effect of MTX. The net results appear to show that the biological situation resulting from treatment with MTX leads to a reduction of effectiveness of the antioxidant enzyme defence system.
Cell Biochem Funct 1998 Dec
PMID:Methotrexate: pentose cycle and oxidative stress. 985 91

Short term hypoxia induced endothelial cells (ECs) injury, as manifested in increasing lactate dehydrogenase (LDH) release and malondialdehyde (MDA) content, decreasing nitric oxide (NO) production and antioxidant enzyme glutathione peroxidase (GSH-Px) activity and increased intracellular calcium concentration, which were further exaggerated by reoxygenation. Administration of 200 U/ml superoxide dismutase (SOD) before hypoxia could partially prevent EC from such injuries, suggesting that the presence of oxygen free radicals may be one of the main factors involved in hypoxia-reoxygenation injury. The ameliorative effect of SOD in case is obviously due to elimination of oxygen free radicals.
Sheng Li Xue Bao 1997 Dec
PMID:[Protection of superoxide dismutase on hypoxia-reoxygenation injury to endothelial cell]. 986 86

After an ischemic episode induced by the electrocoagulation of the left middle cerebral artery (MCA) in mouse, neurons within the damaged territory die either by an apoptotic or by a necrotic process. Most of the cortical neurons within the ischemic area display both morphological and biochemical signs of programmed cell death: nuclear condensation, DNA degradation, formation of apoptotic bodies, and glutathione depletion. In fact, apoptosis essentially contributes to the expansion of the ischemic lesion and the maximum of damaged territory is reached 24 h postocclusion. Several potentially neuroprotective pathways have been evidenced in different experimental models of ischemia including the activation of antioxidant enzyme activities and/or the recruitment of neurotrophic as well as antiapoptotic factors. In our model of permanent focal ischemia induced by MCA occlusion, we measured the temporal synthesis of nerve growth factor (NGF) and examined the status of antioxidant enzymes as well as Bcl-2 antiapoptotic product. We detected in both cortices a transient increase of NGF which peaks at 6 h. Moreover, we reported that glutathione peroxidase is recruited with a time course which parallels NGF synthesis. Finally, we observed the induction of Bcl-2 in safe neurons; this may represent a self-protective response against ischemia-induced apoptosis. We provide evidence that in a model of permanent focal ischemia, several neuroprotective pathways could be coactivated.
Exp Neurol 1998 Dec
PMID:Recruitment of several neuroprotective pathways after permanent focal ischemia in mice. 987 75


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