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)

This study was carried out in order to determine the role of melatonin in preventing lipid peroxidation due to acute ethanol intoxication. Male Wistar Albino rats, 2.5-3 months old, were divided into two groups. Melatonin (in 1% ethanol, 2 mg kg-1 body weight) was given intraperitoneally (i.p.) for 21 days to experimental rats whereas controls received 1% ethanol only. On day 21, 6 g kg-1 body weight ethanol was injected to half of the animals in each group and the remainder were kept as corresponding controls. Animals were killed 5 h after ethanol injection. Malondialdehyde (MDA), reduced glutathione (GSH) and the antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase and catalase) were determined in liver tissue homogenates. MDA levels were increased whereas GSH levels tend to decrease following alcohol injection. Melatonin administration prior to ethanol did not alter MDA and GSH levels of tissue and among antioxidant defence enzymes studied, only CuZn-SOD was found to be increased in animals that received melatonin + ethanol. According to the findings of this study, melatonin did not appear to have any direct effect on alcohol-induced lipid peroxidation.
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PMID:The effect of melatonin administration on ethanol-induced lipid peroxidation in rats. 950 78

It is generally agreed that lipid peroxides play an important role in the pathogenesis of ethanol-induced cellular injury and that free sulfhydryl groups are vital in cellular defense against endogenous or exogenous oxidants. It has been observed that oxidative stress induces the synthesis of the 70-kDa family of heat-shock proteins (HSPs). Induction of HSPs represents an essential and highly conserved cellular response to a variety of stressful stimuli. In the present study we measured in various brain areas and in liver the intracellular levels of HSP70 proteins, sulfhydryl groups and the antioxidant enzyme status after chronic administration of mild intoxicating doses of ethanol to rats. Expression of HSP70 in response to alcohol administration was particularly high in the hippocampus and striatum. In these brain areas, the increase in HSP70 protein levels occurred in absence of significant changes of antioxidant enzyme activities and was correlated with a marked depletion of intracellular bound thiols and with a decreased susceptibility to lipid peroxidation. Lower levels of HSP70 induction were found in cortex and cerebellum and were associated to decreases in SOD and CAT enzyme activities, with a lower depletion of protein bound thiols and with an increased susceptibility to lipid peroxidation. This study agrees with our previous results performed on acute alcohol intoxication and supports the hypothesis that HSP70 induction protects the different brain areas against oxidative stress.
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PMID:Stress proteins and SH-groups in oxidant-induced cellular injury after chronic ethanol administration in rat. 962 70

This study was designed to investigate the dose as well as time dependent effects of ethanol on testicular antioxidant defense system in rats. Male Fischer 344 rats were administered ethanol at a dose of 2, 4, and 6 gm/kg orally and control received equal volume of saline and sacrificed 1 h after ethanol ingestion. For time course study, animals were administered ethanol 4 g/kg orally and sacrificed at 1.5, 2, 4, and 6 h after ethanol ingestion. Testicular ethanol concentration increased with increasing doses of ethanol. Copper zinc-superoxide dismutase (CuZn-SOD) activity significantly decreased in the testes of rats treated with increasing doses of ethanol whereas manganese-superoxide dismutase (Mn-SOD) activity significantly increased in a dose dependent manner (181, 186, and 195% of control, respectively). Testicular glutathione (GSH) and malondialdehyde (MDA) levels did not significantly alter with increasing doses of ethanol one hour after ethanol ingestion. Ethanol concentration decreased in the testes with an increase in time after ethanol ingestion. Testicular CuZn-SOD activity significantly decreased whereas Mn-SOD activity increased with an increase in time after ethanol ingestion. Testicular catalase (CAT) activity significantly decreased at 2 h postethanol ingestion. Testicular MDA levels significantly increased at 4 and 6 h after ethanol ingestion indicating that end product of lipid peroxidation. MDA, takes considerable time to form in the testes. A significant decrease in the ratios of CAT/Mn-SOD and glutathione peroxidase (GSH-Px)/Mn-SOD in the testes of rat suggests the ability of mitochondria to scavenge reactive oxygen species (ROS). It is suggested that antioxidant enzyme ratios may be used as an important parameter to determine ethanol induced oxidative stress in the tissues.
Alcohol
PMID:Dose and time dependent effects of ethanol on antioxidant system in rat testes. 1045 72

This study investigated the response of the antioxidant defense system in brain subcellular fractions after oral graded doses of ethanol to rat. Four groups of male Fischer-344 rats were orally administered saline, ethanol 2 g, 4 g, and 6 g/kg, respectively, and sacrificed 1 hour post treatment. Brain cytosol, synaptosomes, microsomes and mitochondria were separated by density gradient differential centrifugation and assayed for antioxidant system. A significant and dose-dependent-decrease in superoxide dismutase (SOD) activity was observed in all brain subcellular fractions. Catalase (CAT) activity was significantly decreased in brain mitochondria (67% and 80% of control) at higher doses of ethanol; whereas, CAT activity was significantly increased in cytosol, synaptosomes and microsomes. Glutathione peroxidase (GSH-Px) activity was significantly increased in all brain subcellular fractions except in cytosol at higher dose of ethanol. Malondialdehyde (MDA) content was significantly increased in all brain subcellular fractions showing dose response of ethanol-induced oxidative stress. The increase in MDA levels in the brain synaptosomes and microsomes were higher at 6 g dose of ethanol (155% and 163% of control) when compared to mitochondria and cytosol. Glutathione (GSH) levels were significantly increased in brain cytosol and microsomes at higher dose of ethanol (164% and 159% of control); whereas, the GSH concentration was significantly decreased in brain synaptosomes and mitochondria. The antioxidant enzyme (AOE) activity ratios (GSH-Px/SOD and GSH-Px + CAT/SOD) were dose dependently increased in all brain subcellular fractions, particularly in synaptosomes. The GSH/GSSG ratio was dose dependently increased in brain microsomes. The perturbations in the antioxidant defense system and enhanced lipid peroxidation following graded doses of ethanol ingestion indicate a dose-dependent-oxidative 2133stress response in brain subcellular compartments of rats.
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PMID:Dose response of ethanol ingestion on antioxidant defense system in rat brain subcellular fractions. 1069 79

This study investigated the alterations in levels of glutathione, lipid peroxidation, and antioxidant enzyme activity in the liver, lung, and kidney of rats treated with acute doses of ethanol. Male Fisher-344 rats were randomly divided into four groups, and were treated as follows: (1) vehicle (saline) control; (2) ethanol 2 g/kg, p.o.; (3) ethanol 4g/kg, p.o.; and (4) ethanol 6 g/kg, p.o. The animals were sacrificed 1 h after treatment, and tissues were isolated and analyzed. The hepatic GSH levels significantly decreased (73, 68, and 66% of control) due to ethanol ingestion at 2, 4, and 6g/kg, respectively. The hepatic GSH/GSSG ratio also decreased with increasing doses indicating stress response due to ethanol. The hepatic SOD activity significantly decreased (70, 75 and 71% of control) with graded doses of ethanol ingestion. The hepatic CAT/SOD and GSH-Px+CAT/SOD ratios significantly increased (147, 169 and 177% of control) and (140, 167 and 178% of control), respectively with increasing doses of ethanol. In the lung, graded doses of ethanol increased GSH-Px activity (120, 114 and 141% of control) and decreased GR activity (98, 89 and 89% of control), respectively. The MDA concentrations in the lung also increased after higher ethanol ingestion. Most of the antioxidant enzyme ratios increased with increasing doses of ethanol in the lung. In the kidney, GSH-Px activity increased (139, 119 and 151% of control), whereas GR activity decreased (84, 85 and 83% of control). GSH-Px/SOD and GSH-Px+CAT/SOD ratios increased whereas GR/GSH-Px ratio decreased after graded doses of ethanol. GSH levels in the kidney decreased after ethanol ingestion. MDA concentrations increased with increasing dose of ethanol in the kidney. These results showed the dose dependant and tissue specific changes in the antioxidant system after ethanol ingestion. Ethanol exerts oxidative stress on antioxidant systems of liver, lung and kidney in proportion to the amount of ethanol ingestion.
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PMID:Dose response of ethanol on antioxidant defense system of liver, lung, and kidney in rat. 1082 82

This study was designed to determine the ulcer-protecting effects of rutin, a natural flavone, against gastric lesions induced by 50% ethanol, the experimental model related to lesion pathogenesis with production of reactive species. The possible involvement of sulphydryl compounds (SH), neutrophil infiltration, and the capacity of this flavone to restrain the oxidative process produced in the gastric tissue were also investigated. The levels of thiobarbituric acid (TBA, as index of lipid peroxidation), the myeloperoxidase activity (MPO, as a marker of neutrophil infiltration), the content of mucosal sulphydryls (SH) groups and the activity of glutathione peroxidase (GSH-Px, an important antioxidant enzyme) were determined. Pretreatment with the highest dose of rutin (200 mg/kg), 120 min before 50% ethanol, resulted in the most effective necrosis prevention. TBA reactive substances in the gastric mucosa, were increased by ethanol injury, and this increase was inhibited by the administration of 200 mg/kg of rutin. However, the flavonoid was not able to modify the ethanol-induced neutrophil infiltrate expressed as myeloperoxidase activity. Exposure of the gastric mucosa to 50% ethanol induced a significant diminution in gastric non-protein SH content; this parameter also was not modified by the treatment with rutin. GSH-Px activity decreased in the gastric mucosa after ethanol-treatment. In contrast, rutin at all tested doses induced a significant increase in this enzymatic activity, higher than in control group. These results suggest that the gastroprotective effect of rutin in this experimental model appears through an anti-lipoperoxidant effect, and also by enhancement of the anti-oxidant enzymatic (GSH-Px) activity.
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PMID:Evidence for protective and antioxidant properties of rutin, a natural flavone, against ethanol induced gastric lesions. 1090 45

Patients with chronic alcoholism (PCA) of stage II have increased glutathione reductase (GR) activity in neutrophils, lymphocytes and monocytes compared with that in the cells of healthy donors, but superoxide dismutase (SOD) activity was high in neutrophils and low in lymphocytes and monocytes. One-h incubation of the cells with indomethacin (10(-7) M-10(-3) M) in vitro has shown that the drug does not abolish the effect of ethanol: at all concentrations used it stimulated SOD in neutrophils but in a dose-dependent manner inhibited it in lymphocytes with the maximum at a 10(-3) M concentration compared to the control. The same concentration of indomethacin stimulated GR activity in neutrophils but inhibited it in lymphocytes and especially in monocytes. A conclusion is made that prostaglandins and leukotrienes an regulate antioxidant enzyme activities in the cells of the immunophagocytic system of PCA, and the mononuclear cells are more sensitive to ethanol treatment than neutrophils.
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PMID:[Changes in the activity of antioxidant enzymes in different types of leukocytes in patients with chronic alcoholism]. 1283 67

Aralia elata Seemann is an edible mountain vegetable in Korea containing saponin, alkaloid, palmitic acid, linoleic acid, methyl eicosanoate and hexacosol, and is known to manifest an effect on cardiac infarction, gastric ulcer, colitis, and enervation. This study has examined the effects of Aralia elata Seemann ethanol extract on antioxidant enzyme systems and lipid metabolism in rats along with benzo(a)pyrene (B(a)P) administration. Rats were divided into four groups: control (C), an extract fed group (CE), a B(a)P fed group (CB), and a B(a)P and extract fed group (CBE). The ethanol extracts of Aralia elata Seemann (50 mg/kg body weight) were fed to the rats for 4 weeks by stomach tubing. Extract administration increased the antioxidant activities of glutathione sulfur transferase (GST). Total superoxide dismutase (SOD) and Cu,Zn-SOD activities were stimulated. Catalase activities were increased by 50% with extract feeding. Cu,Zn-SOD was greatly enhanced from 0.10 unit to 0.18 unit and catalase activity also was increased. Serum alpha-tocopherol was markedly increased by the extracts. The ethanol fraction of Aralia elata Seemann decreased total serum cholesterol. However, serum HDL-cholesterol was increased by 35% (p<0.05). The results indicate that Aralia elata Seemann exerts antioxidant and strong hypocholesterolemic and hypolipidemic effects in vivo with the administration of B(a)P.
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PMID:Ethanol fraction of Aralia elata Seemann enhances antioxidant activity and lowers serum lipids in rats when administered with benzo(a)pyrene. 1451 64

CYP2E1 induction by ethanol is one mechanism by which ethanol creates oxidative stress in the liver. The superoxide dismutases (SODs) are an important antioxidant enzyme defense system against reactive oxygen species (ROS). To investigate the protective role of SOD against CYP2E1-dependent toxicity, a transfected HepG2 cell line overexpressing CYP2E1 (E47 cells) was infected with adenoviral vectors containing Cu/Zn-SOD complementary DNA (cDNA) (Ad.SOD1) and Mn-SOD cDNA (Ad.SOD2). Forty-eight hours after infection, intracellular levels and activity of Cu/Zn-SOD and Mn-SOD were increased about 2- and 3-fold, respectively. Localization of the overexpressed Cu/Zn-SOD in the cytosol and Mn-SOD in the mitochondria was confirmed by assaying the levels and activity of SOD in the corresponding isolated fractions. Arachidonic acid (AA) plus iron-induced cell death was partially prevented in both Ad.SOD1- and Ad.SOD2-infected E47 cells. Overexpression of Cu/Zn-SOD and Mn-SOD also partially protected E47 cells from the increase in reactive oxygen production and lipid peroxidation and the loss of mitochondrial membrane potential induced by AA and iron. Infection with Cu/Zn-SOD and Mn-SOD also protected the E47 cells against AA toxicity or buthionine sulfoximine (BSO)-dependent toxicity. CYP2E1 levels and catalytic activity were not altered by overexpression of Cu/Zn-SOD or Mn-SOD. Cu/Zn-SOD in the cytosol and Mn-SOD in mitochondria each are capable of protecting HepG2 cells expressing CYP2E1 against cytotoxicity induced by pro-oxidants. In conclusion, these enzymes may be useful in the prevention or improvement of liver injury produced by agents known to be metabolized by CYP2E1 to reactive intermediates and to cause oxidative stress.
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PMID:Adenovirus-mediated expression of Cu/Zn- or Mn-superoxide dismutase protects against CYP2E1-dependent toxicity. 1457 53

Garlic oil was evaluated for gastroprotective activity against ethanol induced ulcers. Reactive oxygen species are involved in the pathogenesis of these ulcers. The possible involvement of garlic oil in restraining the oxidation process produced in gastric tissue was also investigated. The ulcer index, lipid peroxidation and antioxidant enzyme activity (GPx, catalase, SOD) were determined. Pretreatment with garlic oil in doses of 0.25 and 0.5 mg/kg, 30 min before administration of ethanol (1 mL of 100%) caused a decrease in ulcer index and lipid peroxidation and ameliorated the decrease in antioxidant enzyme levels caused by ethanol. The result suggests that garlic oil possesses antioxidant properties and provides protection against ethanol induced gastric injury.
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PMID:Effect of garlic oil on ethanol induced gastric ulcers in rats. 1475 Feb 8


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