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)

Vitamin E and selenium (Se) interact synergistically as an important antioxidant defense mechanisms. Se, an essential component of glutathione peroxidase (GSH-Px) and vitamin E decompose fatty acid hydroperoxides and hydrogen peroxides generated by free radical reactions. Vitamin E and GSH-Px may modulate arachidonic acid metabolism and the activity of cyclooxygenase enzymes by affecting peroxide concentration. The balance between arterial wall prostacyclin (PGI2) production and platelet thromboxane (TX)A2 directly influences platelet activity. In order to elucidate the differential role of dietary vitamin E and Se in aortic PGI2 and platelet TXA2 synthesis, 1-mo-old F344 rats were fed semipurified diets containing different levels of vitamin E (0, 30, 200 ppm) and Se (0, 0.1, 0.2 ppm) for 2 mo. Thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, were measured by radioimmunoassay (RIA) after incubation of whole blood and aortic rings at 37 degrees C for 10 and 30 min, respectively. Vitamin E deficiency reduced plasma vitamin E to 5-17% of control-fed rats, and supplementation in vitamin E-supplemented animals increased plasma GSH-Px by 17%, compared to vitamin E-deficient rats. Se and vitamin E supplementation did not have a similar effect on TXB2 and PGI2 synthesis. Se deficiency did not alter platelet TXB2 synthesis, but significantly decreased aortic PGI2 synthesis. It was necessary to supplement with both antioxidants in order to increase PGI2 synthesis. Se and vitamin E deficient groups had a higher TXB2/PGI2 ratio (0.17 +/- 0.08) compared to Se- and vitamin E-supplemented groups (0.03 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of the platelet thromboxane A2 and aortic prostacyclin synthesis by dietary selenium and vitamin E. 137 63

The role of oxygen derived free radicals or tissue lipid peroxides in the pathogenesis of chronic pancreatitis has not been established. To evaluate long-term effects of tissue lipid peroxides in the pathogenesis of chronic pancreatitis, we treated Wistar male rats with 2,2'-azo-bis-(2-amidino-propane) dihydrochloride (AAPH) and/or linoleic acid (LA) for 3 or 6 months. Rats were divided into eight groups. A: Saline-treated rats for 3 months as control, B: AAPH 40 mg/kgw intraperitoneally, twice a week for 3 months, C: LA 0.5 ml/kgw intraperitoneally, every other week for 3 months, D: AAPH and LA for 3 months, E: Saline-treated for 6 months, F: AAPH for 6 months, G: LA for 6 months, H: AAPH and LA for 6 months. The results were as follows: Lipid peroxide contents of the pancreas were elevated in groups: C, D, G and H. Histological examination revealed epithelial hyperplasia of large pancreatic ducts, vacuolization of ductal epithelium, intraepithelial neutrophilic infiltration, periductal mononuclear cell infiltration (ductulitis and peri-ductulitis), and sporadically in the lobules, destruction of acinar cells, neutrophilic infiltration and ductular proliferation in the same groups. These findings indicate that tissue damage was more severe in the pancreatic ducts than in the acinar cells, however no damage was seen in the endocrine pancreas. Vitamin E content of the pancreas was decreased in groups: B, C, D, F, G and H. Tissue glutathione peroxidase (GSH-Px) activity was increased in groups: D and H. Tissue catalase activity was increased in groups: D, G and H, but no change of superoxide dismutase (SOD) activity was seen in any of the groups. These results indicate that vitamin E may play the role of the main scavenger in the situation of a smaller dose of lipid peroxides, but when larger doses are administered, GSH-Px may play the main role as the scavenger in this experimental system.
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PMID:[Studies on the influence of long-term doses of lipid peroxide generators on rat pancreas]. 140 92

Rats were divided into the following four groups namely (a) sham-operated control, (b) 6-OHDA-treated, (c) sham-operated vitamin E-fed and (d) Vitamin E-fed treated with 6-OHDA. Total glutathione (GSH) and superoxide dismutase (SOD) were measured in brainstem (BS), striatum (ST), hippocampus, frontal cortex, and nucleus accumbens (N. Acc.). GSH and SOD levels were significantly decreased in all regions of 6-OHDA-treated rats compared to controls. Feeding of vitamin E resulted in a significant reduction of GSH in ST and N. Acc. but caused increases in SOD in BS, ST, and N. Acc. Pretreatment of rats with vitamin E caused significant attenuation of the effects of 6-OHDA on GSH and SOD in most of the brain regions. These results show that vitamin E can spare the scavenging systems from the injurious effects of 6-OHDA.
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PMID:Vitamin E attenuates the toxic effects of 6-hydroxydopamine on free radical scavenging systems in rat brain. 142 67

One month-old male Sprague-Dawley rats were maintained on a basal vitamin E-deficient diet supplemented with either 0 or 50 ppm vitamin E for 5 months. Washed red blood cells were resuspended in phosphate buffered-saline, pH 7.4, that contained 0-50 mM glucose and 0-20 mM ethylenediamine tetraacetic acid (EDTA), and were incubated at 37 degrees C for up to 22 h. Contrary to expectations, glucose in the incubation medium accelerated, rather than retarded, the rates of hemolysis, lipid peroxidation and methemoglobin formation in the vitamin E-deficient cells. EDTA, on the other hand, partially inhibited the extent of oxidative damage. Vitamin E-supplemented cells were resistant to oxidative damage in the presence or absence of glucose and/or EDTA. The levels of reduced glutathione (GSH) and activity of catalase were decreased faster in the vitamin E-deficient cells than the supplemented cells, and the rates of their decline were slowed down by either glucose or EDTA. The activities of GSH peroxidase and superoxide dismutase were not significantly altered in the red cells of either group during incubation. The results obtained suggest that reactive oxygen species and reduced metal ions play important roles in initiating oxidative damage to the red cells of vitamin E-deficient rats. However, the agent responsible for initiating the hemolytic event has yet to be established.
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PMID:Oxidative damage in the red cells of vitamin E-deficient rats. 150 85

A 2 x 3 factorial experiment in a randomized complete block design was conducted using a total of 180 weanling pigs in five replicates. The study evaluated the efficacy of two dietary vitamin E sources (D-alpha-tocopherol, DL-alpha-tocopheryl acetate) added at three dietary levels (16, 48, 96 IU/kg) during a 35-d postweaning trial. Pigs within each treatment were fed two similarly fortified vitamin E diets in sequence; the first contained 40% milk products and was fed to 14 d, and the second contained 20% milk product and 5% fat and was provided from 15 to 35 d postweaning. Five pigs per pen per replicate were bled weekly for serum analysis of alpha-tocopherol, Se, cholesterol, triglyceride, and glutathione peroxidase (GSH-Px) activity. At the end of the trial, one pig per pen was randomly selected and killed with liver, loin, lung, and heart excised and frozen for tocopherol analysis. Postweaning gains, feed intakes, and efficiencies were similar between the two vitamin E sources and at the various dietary levels. Serum tocopherol concentrations were consistently higher when D-alpha-tocopherol was provided. Vitamin E sources and levels had no effect nor did they influence weekly serum Se, cholesterol, or triglyceride concentrations or GSH-Px activity. A serum and tissue interaction (P less than .05) response occurred between dietary vitamin E source x level with alpha-tocopherol concentrations increasing linearly (P less than .01) as dietary vitamin E level increased, but at a higher rate when D-alpha-tocopherol than when DL-alpha-tocopheryl acetate as fed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy of dietary D-alpha-tocopherol and DL-alpha-tocopheryl acetate for weanling pigs. 150 9

The aim of the both experiments was to determine whether selenium or selenium/vitamin E supply of rats significantly influences the most important hematological criteria. With experiment 1 the influence of Se deficiency should be determined at two different times of growing. So 36 weaned rats were divided into 2 groups of 18 animals each, the half of them being decapitated at day 22, the rest on day 45. In experiment 2 with the aim to investigate a combination of deficient, adequate and excessive Se and vitamin E supply 90 weaned rats in 9 groups were decapitated at day 44. The basic diet contained 0.04 mg Se and 8 mg vitamin E per kg dry matter and was supplemented in exp. 1 with 0 mg or 0.2 mg Se and 30 mg vitamin E and in exp. 2 with 0 mg, 0.2 mg or 1.0 mg Se and 0 mg, 30 mg or 200 mg vitamin E. With Se deficiency Se concentration and GSH-Px activity in serum and liver were significantly reduced. With excessive Se supply Se concentration in serum was higher; there was no effect on GSH-Px activity. Vitamin E supply had no influence neither on Se content nor on GSH-Px activity in serum or in liver. In exp. 1 Se deficiency caused no clear changes of the analysed hematological criteria although the increase of MCV (+3%) and hematocrit (+7%) on day 22 and the increase of leucocytes (+43%) and the decrease of MCH (-3%) and MCHC (-6%) on day 45 were statistically significant. In exp. 2 these results could not be repeated. The vitamin E supply was without significant effects on the examined hematological parameters.
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PMID:[Hematological parameters, selenium concentration and glutathione peroxidase activities in serum and the liver of rats at different selenium and vitamin E levels]. 158 85

Under the condition of acute NaNO2 poisoning, the changes of myocardial GSH-Px activity of rats fed a diet composed of grains grown in the endemic region of Keshan disease and the same diet with supplementation of vitamin E or selenium were investigated. By gavage of toxic doses of NaNO2, the myocardial GSH-Px was significantly reduced (P less than 0.05). Vitamin E or selenium supplementation protected the enzyme activity from reducing. It is suggested that the simultaneous action of an increase in selenium and vitamin E intake and a decrease in nitrite intake might greatly prevent the occurrence of Keshan disease.
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PMID:Effect of sodium nitrite on myocardial glutathione peroxidase and protective action of vitamin E and selenium. 178 32

Plasma selenium was determined in 92 elderly women: a marked decrease was observed from the age of 65 years. Se-status in 20 elderly women was explored by investigation of the effects of 30 days' Se-supplementation with enriched tablets (Selevit-E) 66 micrograms per day. Serial determination was performed for Se plasma, e-GSH-Px (glutathione peroxidase), MDA (malondialdehyde) and Vitamin E. Significant changes were observed in Se, e-GSH-Px and MDA.
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PMID:Selenium status and effect of selenium supplementation in a group of elderly women. 182 22

In the companion paper we demonstrated that hepatic vitamin E in rats becomes depleted and extrahepatic pools of vitamin E are altered by treatment with 1,2-dibromoethane (DBE). Vitamin E depletion may be dependent upon initial steps of DBE metabolism that are either oxidative (cytochrome P450 dependent) or conjugative (glutathione transferase dependent). That the liver content of glutathione (GSH) and vitamin E, the plasma concentration of vitamin E, and the serum activities of AST and ALT may be influenced by cytosolic metabolism of DBE was assessed by comparison of findings from rats treated with either 1,2-dichloroethane (DCE) or 1-bromo-2-chloroethane (BCE). The extent of oxidative metabolism was diminished by the use of tetradeutero-DBE (d4-DBE), and the availability of GSH for conjugative metabolism was diminished by pretreatment of rats with L-buthionine-S,R-sulfoximine (BSO) prior to treatment with DBE. Our results indicate that neither DCE nor BCE provokes a liver vitamin E depletion in rats, that d4-DBE treatment hastens but does not enhance the observed hepatic vitamin E depletion by comparison to animals treated with an equimolar dose of DBE, and that BSO pretreatment prevented the hepatic vitamin E depletion observed from animals treated with DBE alone. These results indicate that hepatic vitamin E depletion is the unique sequelae to conjugation of GSH with DBE, and we suggest the reactive episulfonium ion intermediate or a macromolecular adduct of this ion derived from DBE may play a role in liver vitamin E depletion associated with exposure to DBE.
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PMID:Modification of hepatic vitamin E stores in vivo. III. Vitamin E depletion by 1,2-dibromoethane may be related to initial conjugation with glutathione. 189 41

Lipid peroxide production, antioxidant contents and activities of antioxidative protective enzymes were examined in lungs of rats exposed to clean air (control group), 0.05 ppm O3, 0.05 ppm O3 + 0.04 ppm NO2 and 0.05 ppm O3 + 0.4 ppm NO2 for 22 months. The results were compared with our previous data in rats exposed to 0.04 ppm NO2, 0.4 ppm NO2 and 4 ppm NO2 for their life span (Sagai et al., Toxicol. Appl. Pharmacol., 73, (1984) 444-456). TBA values used as an index of lipid peroxidation in the lungs were increased maximally at 9 months, but were decreased below control values in animals exposed for 18 and 22 months. Nonprotein sulfhydryl (NPSH) contents were increased maximally at 9 months, and after 18 and 22 months were decreased significantly below control values. Vitamin E (VE) contents showed a similar trend. On the other hand, enzyme activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione peroxidase measured by using cumene hydroperoxide (cum.OOH) substrate (GPx-cum.OOH), glutathione peroxidase measured by using H2O2 as a substrate (GPx-H2O2), glutathione S-transferase (GSH-Tase) and superoxide dismutase (SOD) did not show any significant changes during this experiment. The results show that lipid peroxidation in lungs was increased synergistically by a combination of NO2 and O3 at ambient levels, and that the time of maximum lipid peroxide production was shorter than with NO2 alone. The protective ability against lipid peroxides was higher with increased lipid peroxide levels, but the inducibility was not maintained through a life span exposure to the combined gases. Additionally, two small adenomas were observed in 2 out of 18 rats in the 0.05 ppm O3 + 0.04 ppm NO2 group and a large adenoma was observed in 1 out of 18 animals in the 0.05 ppm + 0.4 ppm NO2 group exposed for 22 months.
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PMID:Biochemical effects of combined gases of nitrogen dioxide and ozone. IV. Changes of lipid peroxidation and antioxidative protective systems in rat lungs upon life span exposure. 201 15


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