Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.3.5.1 (succinate dehydrogenase)
8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Taking into account the found earlier relation of vitamin E to the ubiquinone functioning and metabolism, the authors studied the enzymic activity of succinate dehydrogenase, NADH-dehydrogenase and cytochrome-c-oxidase--coenzyme Q binding sites of the respiratory chain of the rat liver mitochondria. The experiments were carried out with female rats who received a vitamin-E-deficient diet for 6 months. The enzymic activities and the ubiquinone content in the liver mitochondria of these animals are shown to be considerably lower as compared to the animals received a vitamin E diet; alpha-ocopherol, alpha-tocopheronolactone and ubiquinone 3h after administration manifest a clearly pronounced normalizing effect relative to both the enzymic activity and the ubiquinone content. An assumption is advanced that the effect of alpha-tocopherol and its metabolite is associated with controlling the level of functionally active ubiquinone in the mitochondria. Other mechanisms of the membrane-bound enzymes control by the compounds under study are also discussed in connection with the alpha-tocopherol effect on the mitochondrial membranes.
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PMID:[Activity of certain redox enzymes of rat liver mitochondria at different levels of dietary vitamin E]. 22 6

Myocardial infarction was induced in rats by ligating a coronary artery. During a week they received daily injections of 50 mg/kg of vitamin E intramuscularly or 30 mug/kg of sodium selenite subcutaneously, or else a combination of these preparations. The control animals received no injections. Stereometrically a statistically significant reduction of the infarcted zone was noted under the effect of selenium, this reduction being especially distinct during the ischaemic stage; the maturation of granulation tissue with an enhancement of the fibroblast reaction therein was accelerated. The muscle cells of the myocardium beyond the infarction zone displayed an increased activity of lactate dehydrogenase and a reduced activity of succinate dehydrogenase, intactness of the ultrastructure of the cell pattern, an enhancement of the signs of ultrastructural regeneration. Vitamin E potentiated the effect of selenium and executed itself a similar, but less distinct effect.
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PMID:[Morphologic indices the influence of selenium and vitamin E on the course of experimental myocardial infarct]. 101 63

This study compares the toxic effects of the carotenoids, beta-carotene and canthaxanthin, and alpha-tocopherol (vitamin E) on human tumor cells and their normal counterparts in vitro. Seven different malignant cell lines were examined: oral carcinoma (two cell lines), breast (two cell lines), lung carcinoma (two cell lines), and malignant melanoma. The in vitro cell culture assays showed a consistent morphologic change in the affected tumor cells following treatment with carotenoid or vitamin E. A rounding of the tumor cells and eventual lifting off the tissue culture plate were observed. These changes were apparent after 1 to 5 hours of treatment depending on the tumor cell line. Associated with these observable cellular changes were quantitative reductions in proliferation (3H-thymidine proliferation) and succinic dehydrogenase activity (MTT assay). In addition, there was a noticeable change in protein expression, with an increased expression of a 70-kD protein following treatment with beta-carotene. This protein was associated with tumor cells showing a decrease in proliferation (oral carcinoma, malignant melanoma) but not with normal keratinocytes or melanocytes. These studies substantiate a selective cytotoxic effect on human tumor cell growth by carotenoids and alpha-tocopherol in vitro, and may provide an explanation of the therapeutic activity of these agents and their possible use in the treatment of premalignancy or early oral carcinoma.
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PMID:The selective cytotoxic effect of carotenoids and alpha-tocopherol on human cancer cell lines in vitro. 154 92

The protective effects of vitamin E (VE) and selenium (Se) on myocardial mitochondria were investigated in rats fed grains (with 0.006 ppm Se) from an endemic area of Keshan disease. The results indicated that supplementing the endemic grains with VE or Se (in 150 ppm and 0.1 ppm respectively) elevated, in different degrees, the depressed activities of four myocardial mitochondrial complexes of electron transport, of which the activity of complex II was increased significantly (P less than 0.05). In addition, the activity of Mn- superoxide dismutase was increased and the content of lipid peroxides was decreased in the myocardial mitochondria of rats of both groups with the supplements. The study shows that VE and Se protect the myocardial mitochondria from damage induced by lipid peroxidation in the rats fed grains from Keshan disease endemic areas.
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PMID:[Protective effects of vitamin E and selenium on myocardial mitochondria in rats--a study on the pathogenic factors and pathogenesis of Keshan disease]. 220 65

Levodopa, at concentrations of 0.25 x 10(-4) M or larger, is toxic for the human neuroblastoma cell NB69. Toxicity is associated with high levels of quinones, increased activity of complex II-III, and lack of changes of complex I of the mitochondrial respiratory chain. Deprenyl, which does not alter the production of quinones, has a partial protective effect. Tocopherol, 23 or 115 x 10(-6) M, lacks significant preventive effect on levodopa toxicity, but ascorbic acid, 10(-3) M, prevents levodopa toxicity and quinone formation. Deprenyl, 10(-4) M, provides additional protection in cultures treated with levodopa and ascorbic acid. Our results indicate that ascorbic acid and deprenyl prevent levodopa neurotoxicity by unrelated mechanisms. Both compounds should be considered as complementary drugs to test for slowing the progression of Parkinson's disease.
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PMID:Ascorbic acid protects against levodopa-induced neurotoxicity on a catecholamine-rich human neuroblastoma cell line. 834 Dec 91

Studies have shown that ethanol at moderate concentrations inhibits epidermal growth factor-dependent replication of fetal rat hepatocytes in culture. This may account for the growth/development impairment associated with fetal alcohol syndrome and decreased liver regeneration in alcoholic liver disease. In this study, we further define the mechanism(s) of the negative impact of ethanol on fetal rat hepatocytes and provide evidence that ethanol-induced injury to these cells is associated with membrane damage caused by lipid peroxidation, altered cell glutathione homeostasis and deranged mitochondrial structure and function. Exposure of fetal rat hepatocyte replication to ethanol (2 mg/ml) promptly resulted in blockade of replication, as indicated by a 40% reduction in DNA synthesis (p < 0.05). Assessment of cell injury on the basis of lactate dehydrogenase and ALT leakage indicated a statistically significant but not appreciable effect, whereas 51Cr leakage was more substantially increased (p < 0.05). Within 6 hr of ethanol exposure, superoxide radical levels increased more than twofold (p < 0.05). We noted a 56% increase in levels of diene conjugates, a 131% increase in malonaldehyde concentration and a 66% increase in fluorescent products of lipid peroxidation (all p < 0.05). Glutathione levels were decreased to 47% below control values (p < 0.05). Electron microscopic studies illustrated a slight disruption of mitochondrial structure (enlargement of mitochondria and dilation of cristae). This disruption was accompanied by mitochondrial swelling (increased permeability), altered mitochondrial membrane potential (a 16% decrease in rhodamine uptake), a 28% decrease in succinate dehydrogenase activity and a 30% decrease in cellular ATP level (p < 0.05). Pretreatment of fetal rat hepatocytes with 0.1 mmol/L N-acetylcysteine or S-adenosylmethionine for 24 hr prevented the ethanol-induced reduction of ATP and glutathione levels, essentially restored cell replication, ameliorated 51Cr leakage and decreased malonaldehyde and diene conjugate levels to 41% to 65% and 25% above control values, respectively. Pretreatment with 0.1 mmol/L vitamin E fully normalized malonaldehyde and diene conjugate levels and 51Cr leakage but failed to improve ATP levels or to increase significantly cell replication and glutathione levels. Concomitant administration of glutathione precursors with ethanol, rather than pretreatment, did not alter the impaired cell replication. Thus our data underscore the importance of cellular glutathione and ATP in preventing ethanol-induced decreases in fetal cell replication and suggest that alleviation of cellular lipid peroxidation alone is not sufficient to prevent this abnormality in fetal rat hepatocyte function.
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PMID:Effect of ethanol on rat fetal hepatocytes: studies on cell replication, lipid peroxidation and glutathione. 835 6

Responses of vitamin E-depleted female rats to acute exercise and chronic exercise training were tested. Rats were fed either a control diet (+E rats) or a vitamin E-depleted diet (-E rats). After 8 wk, subgroups of the +E and -E rats performed treadmill exercise for 45 min at 28 m/min, 15% grade, and were immediately killed. Vitamin E concentrations were 80-90% lower in liver, heart and muscles in -E rats as determined by HPLC. There was no difference between +E and -E rats in blood lactate concentration, creatine kinase, lipid peroxidation indices, hematocrit or hemoglobin concentration following acute exercise. Remaining rats were either trained for a further 8 wk at 40 m/min, 15% incline for up to 60 min/d or served as untrained controls. No differences in training tolerance were seen between diet groups, with 64% of +E rats and 71% of -E rats consistently completing 60 min of daily training. The training induced similar adaptive elevations in succinate dehydrogenase activity (31-107%) in various hind limb muscles of both +E and -E rats. Trained +E rats had lower vitamin E concentrations in some but not all tissues when compared with untrained +E controls. These results suggest that consumption of a vitamin E-free diet for 8 wk did not result in differences in blood indices associated with exercise stress or in the ability to perform a submaximal acute exercise test when compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamin E status does not affect the responses to exercise training and acute exercise in female rats. 848 94

Vitamin E (alpha-tocopherol) is a known biological antioxidant able to quench the lipid peroxidation chain and to protect the cellular structures (e.g., plasma membranes) from the attack of free radicals which are reported to play a primary role in aging. To assess whether the absence of alpha-tocopherol from the diet of young laboratory animals may be considered a reliable model of precocious brain aging, intracellular ionic content of brain cortex pyramidal cells, ultrastructural features of synaptic contact zones, synaptic mitochondria and perykarial mitochondria positive to the succinic dehydrogenase (SDH) histochemical reaction with copper ferrocyanide have been investigated by X-ray microanalysis and computer-assisted morphometry in young, adult, old and 11-month-old vitamin E deficient rats. Our data document significant alterations of intracellular ionic content, synaptic contact areas and synaptic and perykarial mitochondria in aging. Vitamin E deficiency caused similar alterations in adult animals. Taking into account the known role of alpha-tocopherol in protecting the cellular membrane structure, we support that the common process underlying the changes found in aging and vitamin E deficiency is an excessive deterioration of the neuronal membrane.
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PMID:Vitamin E deficiency as a model of precocious brain aging: assessment by X-ray microanalysis and morphometry. 855 24

The mechanisms that lead to mitochondrial damage under oxidative stress conditions were examined in synaptosomes treated with ascorbate/iron. A loss of membrane integrity, evaluated by electron microscopy and by LDH leakage, was observed in peroxidized synaptosomes and it was prevented by pre-incubation with vitamin E (150 microM) and idebenone (50 microM). ATP levels decreased, in synaptosomes exposed to ascorbate/iron, as compared to controls. NADH-ubiquinone oxidoreductase (Cx I) and cytochrome c oxidase (Cx IV) activities were unchanged after ascorbate/iron treatment, whereas succinate-ubiquinone oxidoreductase (Cx II), ubiquinol cytochrome c reductase (Cx III) and ATP-synthase (Cx V) activities were reduced by 55%, 40%, and 55%, respectively. The decrease of complex II and ATP-synthase activities was prevented by reduced glutathione (GSH), whereas the other antioxidants tested (vitamin E and idebenone) were ineffective. However, vitamin E, idebenone and GSH prevented the reduction of complex III activity observed in synaptosomes treated with ascorbate/iron. GSH protective effect suggests that the oxidation of protein SH-groups is involved in the inhibition of complexes II, III and V activity, whereas vitamin E and idebenone protection suggests that membrane lipid peroxidation is also involved in the reduction of complex III activity. These results may indicate that the inhibition of the mitochondrial respiratory chain enzymatic complexes, that are differentially affected by oxidative stress, can be recovered by specific antioxidants.
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PMID:Mitochondrial function is differentially affected upon oxidative stress. 989 Jun 35

Correcting action of vitamin E and it's short chain derivative on the activity of some mitochondria electron transport chain enzymes were investigated on models of acute and chronic toxic hepatitis. Inhibition of NADH- and succinate-cytochrome c oxidoreductase complexes activity was established in short term action of xenobiotics. Treatment of rats with CCl4 during 60 days lowered activity of NADH-cytochrome c oxidoreductase complex and significantly increased activity of succinate-cytochrome c oxidoreductase complex and succinate dehydrogenase. Obviously, as a result of long term influence of hepatotoxic agents switching over in rat mitochondria electron transport from NAD-dependent way of substrate oxidation to succinate-dependent way took place. This event could be a part of the body adaptation mechanisms. Vitamin E and its short chain analogue corrected activities of investigated enzymes of mitochondria liver in the animals with acute and chronic hepatitis.
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PMID:[Correction of the activity of certain enzymes in the rat liver mitochondrial electron transport chain by derivatives of alpha-tocopheryl acetate in toxic damage to the liver]. 1079 Oct 53


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