Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1260386 (GSH)
 38,102 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used the apolipoprotein E deficient (apo e-/-) mice to analyze the role of macrophage reduced glutathione (GSH) content in cell-mediated oxidation of LDL and in atherosclerotic lesion development. Apo e-/- mice were supplemented with L-2-oxo-4-thiazolidin carboxylate (OTC, which supplies cysteine residues, 500 mg/kg/day), or with buthionine sulfoximine (BSO, a specific inhibitor of GSH synthesis, 400 mg/kg/day) for 6 weeks. Then mouse peritoneal macrophages (MPM) and the mice aortas were collected. MPM from apo e-/- mice contained decreased GSH levels (by 58%), and a four-fold increased lipid peroxides content compared to control macrophages from C57BL6 mice. These MPM demonstrated increased capability to release superoxide anions and to oxidize LDL in comparison to control MPM. OTC supplementation resulted in a 26% increase in macrophage GSH, paralleled by a 25% reduction in cellular lipid peroxides content. Decrement by 30% in superoxide anion release and LDL oxidation by MPM, and also in the atherosclerotic lesion size by 25%, was found in the OTC-treated mice, compared to placebo-treated apo e-/- mice. In contrast, in BSO-treated mice MPM a further depletion of cellular GSH by 22% was found, paralleled by a two-fold increase in lipid peroxides content, and a 41% increased superoxide anion release and cell-mediated LDL oxidation, compared to placebo-treated apo e-/- mice MPM. Most important, BSO supplementation to apo e-/- mice caused a 59% increase in the atherosclerotic lesion area. An additional way to increase cellular GSH content was the use of dietary antioxidants. Vitamin E (40 mg/kg/day) or the isoflavan glabridin (25 microg/kg/day) administration for 2 months to apo e-/- mice resulted in the accumulation of these antioxidants in their MPM, and increased MPM GSH content by 24 and 80%, respectively. MPM lipid peroxides content was reduced by 31 or 60% upon vitamin E or glabridin supplementation, paralleled by a 30 or 60% decrease in cell-mediated oxidation of LDL, respectively. Finally, a significant inverse correlation (R=0.83) was found between macrophage GSH content and cell-mediated oxidation of LDL. We conclude that enrichment in vivo of macrophages with GSH, significantly decreases cellular oxidative stress, leading to reduced capability of the macrophages to oxidize LDL, and hence GSH may attenuate the development of atherosclerosis.
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PMID:Increased macrophage glutathione content reduces cell-mediated oxidation of LDL and atherosclerosis in apolipoprotein E-deficient mice. 1204 18

Pre-term neonates and neonates in general exhibit physiological vitamin E deficiency and are at increased risk for the development of acute lung diseases. Apoptosis is a major cause of acute lung damage in alveolar type II cells. In this paper, we evaluated the hypothesis that vitamin E deficiency predisposes alveolar type II cells to apoptosis. Therefore, we measured markers of apoptosis in alveolar type II cells isolated from control rats, vitamin E deficient rats and deficient rats that were re-fed a vitamin E-enriched diet. Bax and cytosolic cytochrome c increased, and the mitochondrial transmembrane potential and Hsp25 expression was reduced in vitamin E deficiency. Furthermore, increased DNA-fragmentation and numbers of early and late apoptotic cells were seen, but caspases 3 and 8 activities and expression of Fas, Bcl-2, Bcl-x and p53 remained unchanged. Vitamin E depletion did not change the GSH/GSSG ratio and the activities of antioxidant enzymes. Thus, vitamin E deficiency may induce a reversible pro-apoptotic response in lung cells and sensitise them for additional insult. In agreement with this hypothesis, we demonstrate that in vivo hyperoxia alone does not induce apoptosis in type II cells of control rats but reversibly increases DNA-fragmentation and numbers of early apoptotic type II cells in vitamin E-depleted cells.
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PMID:Vitamin E deficiency sensitizes alveolar type II cells for apoptosis. 1206 53

The ameliorating effects of melatonin and vitamin C plus vitamin E were examined histologically and biochemically in lung tissues in rats exposed to chlorpyriphos-ethyl (CE). Experimental groups were as follows: Control group (C), CE treated group (CE), vitamin C plus vitamin E treated group (Vit), melatonin treated group (Mel), vitamin C plus vitamin E plus CE treated group (Vit + CE), and melatonin plus CE treated group (Mel + CE). Vitamin E and vitamin C were administered intramuscularly at the rates of 150 and 200 mg per kg body weight, respectively, in Vit and Vit + CE groups, once a day for 6 consecutive days. Melatonin was administered intramuscularly at the rate of 10 mg per kg body weight in Mel and Mel + CE groups, once a day for 6 consecutive days. At the end of the fifth day, the rats of CE, Vit + CE and Mel + CE groups were treated orally with CE dissolved in corn oil with two equal doses of 41 mg CE per kg body weight at zero and twenty-first hours. Tissue samples of lungs were taken by using appropriate techniques for biochemical and histological examinations under anesthesia at the twenty-fourth hours of CE administration, at the end of the sixth day of the experiment. In tissue homogenates, the level of thiobarbituric acid reactive substances (TBARS), antioxidant potential (AOP), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were determined. TBARS was significantly high (p < 0.05) in CE group compared to control group, while TBARS was found to significantly decrease (p < 0.05) with Vit and Mel groups compared to control. On the other hand, TBARS was seen to significantly decrease (p < 0.05) in both groups of Vit + CE and Mel + CE compared to CE group. In comparison with CE group, SOD activity was significantly high (p < 0.05) with the groups of Vit, Mel, Vit + CE and Mel + CE. GSH-Px activity was found to significantly decrease (p < 0.05) with CE group, compared with both C and Vit groups. AOP was significantly lower (p < 0.01) in CE group than C group. Although there was an increased AOP with Vit + CE and Mel + CE groups compared to CE group, the increase in AOP was only seen to be significant (p < 0.05) in Mel + CE group. In comparison with C group, AOP significantly (p < 0.05) increased with Vit group. There was also a significant (p < 0.05) increase in AOP with Mel + CE group, compared with CE group. Additionally, AOP was significantly lower (p < 0.05) in Vit + CE group than Mel + CE group. Lungs were examined histologically at the end of sixth day. There were remarkable changes in the histomorphology of peribronchial and perivascular area in the lung of rats treated with CE. These were infiltration of mononuclear cells (such as lymphocytes, plasmocytes, macrophages), hyperplasia of type II pneumocyte, and thickened and increased connective tissue. Damage to the lung tissue such as increased inflammatory mononuclear cells in peribronchial and perivascular areas were more pronounced for the CE group than Vit + CE and Mel + CE groups in which these changes were higher than C, Vit and Mel groups. These results suggest that CE increases lipid peroxidation and decreases antioxidant enzymes activities and AOP due to increasing oxidative stress induced by CE, and high doses of vitamin C plus vitamin E and melatonin considerably reduce CE toxicity in lung tissues of rats.
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PMID:Protective role of melatonin and a combination of vitamin C and vitamin E on lung toxicity induced by chlorpyrifos-ethyl in rats. 1221 44

The aim of this study was to determine the effects of Hippophae rhamnoides L. extract (HRe-1) and also vitamin E as a positive control on nicotine-induced oxidative stress in rat blood, specifically alterations in erythrocyte malondialdehyde (MDA) level, activities of some erythrocyte antioxidant enzymes, and plasma vitamin E and A levels. The groups were: nicotine (0.5 mg/kg/d, intraperitoneal, i.p.); nicotine+vitamin E (75 mg/kg/d, intragastric, i.g.); nicotine+HRe-1 (1 ml/kg/d, i.g.); and control group (receiving only vehicles). There were 8 rats per group and the supplementation period was 3 weeks. Nicotine-induced increase in erythrocyte MDA level was prevented by both HRe-1 and vitamin E. Nicotine-induced decrease in erythrocyte superoxide dismutase (SOD) activity was prevented by HRe-1, but not vitamin E. HRe-1 increased the erythrocyte glutathione peroxidase (GSH-Px) activity compared with nicotine and the vitamin E groups. Catalase activity was not affected. Vitamin E supplementation increased plasma vitamin E level. Plasma vitamin A level was higher in both vitamin E and HRe-1 supplemented groups compared with nicotine and control groups. The results suggest that HRe-1 extract can be used as a dietary supplement, especially by people who smoke, in order to prevent nicotine-induced oxidative stress.
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PMID:Beneficial effects of Hippophae rhamnoides L. on nicotine induced oxidative stress in rat blood compared with vitamin E. 1223 Jan 3

Quinolones (Qs) were shown to have cytotoxic effects in various cell lines including human carcinoma cells; however, mechanism of these effects was not fully understood. To investigate the possibility of the involvement of an oxidative stress induction in this mechanism of action, we examined viability of human fibroblast cells exposed to a Q antibiotic, ciprofloxacin (CPFX), and measured lipid peroxidation and total glutathione (GSH) levels, and activities of catalase (Cat), superoxide dismutases (SODs), glutathione peroxidase (GPx). The effects of vitamin E pretreatment on those parameters were also examined. Our results showed that the effect of CPFX on the viability of the cells, as determined by neutral red uptake assay, was time dependent. Cytotoxicity was not observed in the concentration range of 0.0129-0.387 mM CPFX when the cells were incubated for 24 hours. However, significant level of cytotoxicity was observed at concentrations 0.129 and 0.194 mM, and >0.129 mM, following 48 and 72 hours of exposure, respectively. When the cells were exposed to 0.194 mM CPFX for 48 hours, the level of lipid peroxidation increased and the content of total GSH decreased significantly; activities of total SOD, Mn SOD and CuZn SOD did not change; the decrease observed in the activity of Cat was not significant; and the activity of GPx was highly variable. Vitamin E pretreatment of the cells provided significant protection against CPFX-induced cytotoxicity; lowered the level of lipid peroxidation significantly, but increased the total GSH content only moderately; no change was observed in the activities of Cat and total SOD, but a significant increase in Mn SOD and a significant decrease in CuZn SOD were noticed. These results suggested that CPFX-induced cytotoxicity on human fibroblast cell cultures is related to oxidative stress, and vitamin E pretreatment can afford a protection.
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PMID:Cytotoxicity in ciprofloxacin-treated human fibroblast cells and protection by vitamin E. 1254 33

The anti-oxidative effect of proanthocyanidins(PC) was evaluated in D-galactose-induced murine model. Male KUNMING mice were divided into different groups at random. The mice were induced by subcutaneous injection of D-galactose on the back of mice daily for 60 days and simultaneously PC and VE were administered to the mice by oral feeding. Results indicate that the lipid peroxide in blood, liver and brain significantly increased respectively because of the D-galactose injection, when compared to the control. The activity of SOD in RBC and liver significantly decreased while that of GSH-PX in blood and liver decreased. MAO-B in brain was significantly increased while MAO-B in liver doesn't change significantly. Oral feeding PC markedly decreased the formation of MDA in blood, liver and brain, increased the activities of SOD in blood and liver and decreased the activity of MAO-B in brain. Vitamin E also counteract the oxidative stress induced by D-galactose. In summary, treatment with PC at all the three tested doses were effective in exerting a protective effect against oxidative stress.
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PMID:[Anti-oxidative effects of proanthocyanidins in mice induced by D-galactose]. 1254 59

The Vitamin E (VE) effect was examined on oxidative damage to DNA, lipids, and protein in mice that were fed various levels of lipid diets after total body irradiation (TBI) with X-rays at 2 Gy. No increase of 8-hydroxydeoxyguanosine (8OHdG) by TBI was observed in the + VE group; however, in the case of the -VE group, a significantly higher 8OHdG level was observed in the high-lipid group than in the low- or basal-lipid group. In the groups with TBI, the concentration of thiobarbituric reactive substances (TBARS) only significantly increased in the high-lipid (-VE) group. These changes in TBARS, due to TBI, were not detected in other groups. The contents of protein carbonyls only increased in the (-VE) group. The contents of protein carbonyls was significantly different between the (+VE) and the (-VE) groups, regardless of the lipid levels. The concentrations of GSH, vitamins C and E in the liver were lower, and the concentration of non-heme iron in the liver was higher in the high-lipid group than in the low- and basal-lipid groups. These concentrations in the high-lipid group were significantly different between the (+VE) and the (-VE) groups. These results strongly suggest that mice that are fed a high-lipid diet are susceptible to TBI-induced oxidative damage. Also, decreases in the GSH levels and an increase in the iron level are involved in the mechanism of this susceptibility.
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PMID:Vitamin E modulates radiation-induced oxidative damage in mice fed a high-lipid diet. 1268 18

Halothane, commonly used for anesthetizing humans and animals, is one of the most important volatile anesthetics and may cause the formation of free radicals during its biotransformation. Free radicals may lead to degeneration of liver cells. Vitamin E and glutathione peroxidase (GSH-Px) containing selenium are two natural antioxidants, and these may protect the cellular lipid and lipoproteins against oxidative damage caused by free radicals. Therefore, the purposes of the present study were to investigate the probable protective effects of intraperitoneally administered Se and vitamin E on liver enzymes and to determine some other hematological parameters in the halothane anesthesia of rats. All rats were randomly divided into five groups. The first group was used as a control, and physiological saline (0.9%) was intraperitoneally injected into these animals as a placebo. The second group was used as an anesthesia control group and was only anesthetized with halothane for two hours. The third group received intraperitoneally administered Se (Na2SeO3, 0.3 mg/200 g body weight), the fourth group vitamin E (dl-alpha-tocopheryl acetate, 100 mg/kg body weight), and the fifth group a Se plus vitamin E combination (Na2SeO3, 0.3 mg/200 g body weight + dl-alpha-tocopheryl acetate, 100 mg/kg body weight). The activities of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase, triglycerides, erythrocyte counts, the packet-cell volume, hemoglobin concentrations and neutrophyle rates significantly increased (p < 0.05 to p < 0.01) after halothane anesthesia and returned to near control levels after Se, vitamin E and Se plus vitamin E injections. The values of cholesterol, total protein, white blood cell counts and lymphocyte rates significantly decreased (p < 0.05 to p < 0.01) in the anesthesia control group. However, the levels of albumin, total bilirubin, creatinine, the mean corpuscular volume, the mean corpuscular hemoglobin, and the mean corpuscular hemoglobin concentration were not statistically influenced. In conclusion, we have determined that halothane anesthesia affected some liver enzymes and some other biochemical and hematological parameters. Se, vitamin E and their combination may prevent the increase of liver enzymes after halothane anesthesia. Based upon these results, Se and vitamin E may play an important role in the indication of hepatic cellular injury produced by halothane.
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PMID:Effects of intraperitoneally injected selenium and vitamin E in rats anesthetized with halothane. 1275 99

With the aim of evaluating the effect of interaction between physical training or exercise only during pregnancy and thermal stress on oxidative stress, and antioxidant mechanism sedentary pregnant rats (PS), exercised pregnant rats only during pregnancy (PE) and trained rats submitted to also exercise during pregnancy (PT) were compared (N=63). Exercise sessions consisted of swimming at 80% of maximal work load supported into water at 28 degrees C (hypothermia, PS 28, PE28, PT28) or 35 degrees C (thermal neutrality, PS35, PE35, PT35) or 39 degrees C (hyperthermia, PS39, PE39, PT39), for 30 min. The initial body weight in all groups of rats was from 177 to 207 g. On the 20th day of pregnancy, 24 h after the last immersion or swimming session venous blood was collected to determine oxidative stress. Plasma concentrations of means malondialdehyde (MDA) values measured as thiobarbituric acid reactive substances (TBARS); total glutathione (GSH) and vitamin E were determined. The oxidative stress index was calculated from the ratio TBARS/GSH and TBARS/Vitamin E. TBARS did not change on the group PE at different temperatures of water; TBARS were higher for PS28 than PS35 and PS39; PT35 had higher values than PT28 and PT39. For GSH, PS39 was lower than PS35; PE28 was higher than PE35 and PE39 and PT35 were lower than PT28 and PT39. Plasma concentration of vitamin E did not present any difference for sedentary rats at different water temperatures, but for PE28, the values were lower than for PE35 and PE39, whereas PT39 was lower than PT35 and PT28. In relation to TBARS/GSH, it was verified an increase in oxidative stress for PS28 (in relation to PS35 and PS39), PE35, and PT35 (in relation to PE28 and PE39 or PT28 and PT39); regarding the ratio TBARS/vitamin E, the highest values were obtained at 35 degrees C for PS and PT groups and at 39 for PE group. These results have shown the great complexity of the interaction between physical training, thermal stress and pregnancy. Apparently, hypothermia produces large index of oxidative stress only in sedentary rats, but this index was greater at 35 degrees C in relation to extreme temperatures for trained rats. These results have suggested that physical training allows a more efficient activation of antioxidant mechanisms under thermal stress.
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PMID:Reactive oxygen species in pregnant rats: effects of exercise and thermal stress. 1278 44

Methanol is primarily metabolized by oxidation to formaldehyde and then to formic acid. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports the in vitro antioxidant effect of vitamin E on isolated hepatocytes of folic acid deficient rats rendered so as to emulate a human hepatocyte model. These hepatocytes were treated with 320 microM of methanol per million cells and incubated for 30 min. The microsomal fraction of these hepatocytes showed a decreased level of superoxide dismutase (SOD), with increase in lipid peroxidation (LPO) shown by increase in recorded levels of malondialdehyde (MDA). Catalase activity was shown to be increased. Levels of reduced glutathione (GSH) were decreased and the activity of glutathione peroxidase (GSH-Px) and of glutathione reductase (GSSG-R) were not altered. The hepatocytes of folate deficient rats pretreated with vitamin E, when subjected to methanol treatment, showed no significant change in SOD levels and a significant decrease in MDA levels. The catalase activity in this group of animals showed a highly significant decrease. These animals had normal levels of GSH, while a significant fall in GSH-Px and GSSG-R levels were observed. These results suggest that Vitamin E exerts a protective effect on hepatocytes by acting as a free radical scavenger, proving its usefulness in treating methanol toxicity.
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PMID:In vitro effect of methanol on folate-deficient rat hepatocytes. 1282 Dec 9


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