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)

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

The present investigation was undertaken to examine the biochemical changes occurring in blood and tissues of Landrace pigs given intravenously 2 mg selenium/kg b.w. as either sodium selenite or dimethylselenide. NADP-isocitric dehydrogenase, lactic dehydrogenase and succinic dehydrogenase activities were evaluated in subcellular fractions from liver, heart (right and left ventricle) kidney and longissimus dorsi. Other tested parameters included plasma cations and proteins, blood urea nitrogen, hematocrit as well as selected serum enzymes. The marked inhibition of succinic dehydrogenase along with the rise of the two other dehydrogenases and the modification of the plasma cation profile suggest that in swine sodium selenite may act by determining a shift toward anaerobiosis accompanied by alterations in cell membrane permeability. Comparatively, dimethylselenide was found to affect the tissue enzymes to a similar but less severe extent and appeared devoid of significant effects on the remaining parameters. The possible relationships between the cardiovascular alterations brought about by sodium selenite (described elsewhere) and the observed biochemical changes in the present study are finally discussed.
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PMID:Pathogenesis of sodium selenite and dimethylselenide acute toxicosis in swine: tissue and blood biochemical changes. 215 34

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

Keshan disease (KD) is a cardiomyopathy endemic in certain areas of China, characterized by severe deterioration and multiple focal necrosis. In the present paper we describe abnormalities of the structure and function of myocardial mitochondria from patients with subacute Keshan disease. Activities of succinate dehydrogenase, succinic oxidase, cytochrome c oxidase, H(+)-ATPase and its sensitivity to oligomycin and the response of membrane potential to energization by ATP were significantly decreased. However, the spectrum of reduced-minus-oxidized cytochromes in patients' mitochondria showed no obvious difference in the content of cytochrome c oxidase (aa3). There was also a marked decrease in lipid fluidity of affected mitochondria, and an abnormal amount of moderately electron dense amorphous inclusions. Electron-microscopic x-ray microanalysis and exposure to protein digestion reagent demonstrated that these inclusions are not Ca3(PO4)2, but are, probably, proteinaceous in nature. Affected mitochondria had markedly decreased selenium content. The defects in myocardial mitochondria from patients with chronic Keshan disease were less extensive than those in patients with subacute Keshan disease. We propose that Keshan disease be classified as a form of "mitochondrial cardiomyopathy".
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PMID:Keshan disease--an endemic mitochondrial cardiomyopathy in China. 290 94

Male albino mice were pair-fed a torula yeast-based selenium-deficient (Se-) diet containing 10 ppb selenium for 4 months, while a control group (Se+) received a similar diet supplemented with 330 ppb selenium as Na2SeO3. In addition to previously observed modulations of drug-metabolizing enzymes (Reiter, R. and Wendel, A. (1985) Biochem. Pharmacol. 34, 2287-2290), an increase of 6-phosphogluconate dehydrogenase activity and succinate dehydrogenase activity in liver by about 60% was found. In vivo, an increased 14CO2 exhalation from a tracer dose of glucose either labeled in the C-1- or C-6 position was observed in selenium-deficient mice. However, no difference in the total CO2 exhalation of Se(-)- as compared to Se+-mice was detectable. In line with the assumption that Se(-)-mice have an increased glucose turnover, Se(-)-mice exhibited a greater glucose tolerance when treated with an oral glucose load of 2.5 mg glucose/kg body weight. Also, the Se(-)-mice had a lower blood glucose level as compared to Se+-controls (89 +/- 3 versus 110 +/- 12 mg glucose/100 ml blood). Further in vitro experiments with red blood cells from Se(-)-mice showed that erythrocytes did not contribute to an increased CO2 formation from glucose via the pentose phosphate shunt. No significant differences between Se(-)- and Se+-animals were found in the profile of urinary metabolites, including ketone bodies and nitrogen excretion. These findings suggest a hitherto unknown involvement of selenium in specific regulatory sites of intermediary metabolism.
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PMID:Alterations in the intermediary metabolism of selenium-deficient mice. 311 95

The effects of selenium on 7,12-dimethylbenzanthracene-induced mammary tumorigenesis were examined in C57BL X DBA/2f F1 mice fed a semipurified diet. Mice fed 0.2 ppm selenium developed 56% mammary tumors; in contrast, mice fed 2.0 ppm selenium developed only 16% mammary tumors at 11 months of age. Mice fed the 2.0-ppm selenium diet grew as well as did their counterparts fed the 0.2-ppm selenium diet. In a separate experiment, the level of selenium-dependent glutathione peroxidase was measured in the mammary glands of control and 7,12-dimethylbenzanthracene-treated BALB/c mice fed basal and selenium-supplemented diets. 7,12-Dimethylbenzanthracene treatment resulted in decreased glutathione peroxidase activity n mice fed both low (0.03 ppm)- and high (1.50 ppm)-selenium diets. Thus, the chemopreventive effects of selenium could not be attributed to maintaining high levels of glutathione peroxidase. In a second series of experiments, the effects of selenium were further examined on the growth of mammary cell line YN-4 in monolayer cell culture. The mitochondrial inclusions seen in cells exposed to 5 X 10(-6) M selenium could not be correlated with changes in the activity of the mitochondrial enzymes, cytochrome c oxidase and succinate dehydrogenase, thus implying that there was no demonstratable impairment of mitochondria. The examination of selenium-treated cells with flow cytofluorometry indicated that cells were blocked in S-G2 phases of the cell cycle. This latter result illustrates one feasible approach towards identifying specific mechanisms for the chemopreventive effects of selenium.
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PMID:Selenium and mouse mammary tumorigenesis: an investigation of possible mechanisms. 640 37

The different effects of lead exposure in young children and adults, and inconsistencies between in vivo and in vitro studies as well as between experimental and clinical data suggest that lead toxicity may have different mechanisms. During the developmental phase, lead neurotoxicity results in permanent dysfunction, but its neuropharmacological toxicity as seen in adults might involve its interaction with micronutrients such as calcium and zinc. Lead administered orally in a dose of 20 mg/kg for 8 weeks was found to inhibit the enzyme activity of succinic dehydrogenase, acetylcholine esterase and Na+/K+ ATPase both in the cerebrum and in the cerebellum. Selenium also affected these enzymes when administered in a dose of 0.5 ppm for 8 weeks. When lead and selenium were administered simultaneously the inhibition of the three enzyme activities was considerably alleviated. However, when selenium (0.5 ppm) was given only for 15 days after exposure to lead, the activity of the enzymes was much reduced when compared with control.
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PMID:Effect of selenium on lead-induced neurotoxicity in different brain regions of adult rats. 765 36

The metabolic significance of Se in plants is not well documented, though the presence of many selenoenzymes in bacteria and the essentiality of Se in higher animals is established. Since germination is an active process in plant growth and metabolism, the effect of Se was investigated in germinating Vigna radiata L, a nonaccumulating Se-deficient legume. Growth and protein were enhanced in seedlings supplemented with selenium (Se) as sodium selenite in the medium up to 1 microgram/mL. The pattern of uptake of 75Se in the differentiating tissues and the subcellular distribution were investigated. The percentage of incorporation of 75Se was greater in the mitochondria at the lowest level (0.5 micrograms/mL) of Se supplementation compared to higher levels of Se exposure. Proteins precipitated from the postmitochondrial supernatant fractions, when separated by means of polyacrylamide gel electrophoresis (PAGE), indicated a major selenoprotein in the seedlings germinated at 2.0 micrograms/mL Se. In seedlings grown with supplemented Se, enhanced respiratory control ratio and succinate dehydrogenase activity were observed in the mitochondria of tissues, indicative of a role for Se in mitochondrial membrane functions.
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PMID:Subcellular distribution of selenium during uptake and its influence on mitochondrial oxidations in germinating Vigna radiata L. 766

Previous studies have shown the pathogenic effects of grains cultivated in the endemic areas of Keshan disease and selenium is effective in the prevention of this disease. In this study, liver damages induced by feeding grains from an endemic area (endemic diet), and the effects of selenium and alpha-tocopherol supplement were examined. After 3 months on the endemic diet, the amounts of serum enzymes were significantly increased when compared to controls (animals receiving diet from a non-endemic area). Liver enzymes (alkaline phosphatase and choline esterase) were also found to be altered in the serum, further suggesting liver damages in animals on an endemic diet. Supplement of the endemic diet with selenium or alpha-tocopherol reversed the changes in serum enzymes. Increase in lipid peroxidation in the liver of animals on the endemic diet was observed when compared to that in control animals. Selenium and alpha-tocopherol supplements prevented the increase in lipid peroxidation in the liver by the endemic diet. Semi-quantitative histochemical analysis of glutamate dehydrogenase and succinate dehydrogenase in liver tissue showed that the livers of animals on an endemic diet were more sensitive to ischemic damages in vitro. Supplementation of the endemic diet with either selenium or alpha-tocopherol reduced the sensitivity to ischemic damages. The results suggest that increased lipid peroxidation in the liver of rats on an endemic diet may be responsible for liver damages and elevation of serum enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of selenium and alpha-tocopherol on liver damage induced by feeding grains from an endemic area of Keshan disease in rats. 796 93

The purpose of this study was to examine the changes induced by endurance training, with or without selenium (Se) supplementation on: 1) mitochondrial activity of succinate dehydrogenase (SDH) and cytochrome c oxidase (Cyt Ox),2) the myosin heavy chain (MHC) expression in muscle fibers and 3) their association with aerobic performance. Twenty-four male students volunteered to participate in this double blind study: selenium (Sel, N = 12) vs placebo (Pla, N = 12). During a 10-wk endurance training program, the Sel group received a daily Se supplementation containing 180 micrograms of organic selenium (selenomethionine), while the Pla group received a placebo. Before (Pre) and after (Post) the program (3 sessions wk-1) an endurance exercise (Capmax) was performed in order to determine the aerobic endurance capacity assessed by the total oxygen uptake during the running test (VO2tot). All parameters of aerobic performance were increased in both groups, concomitantly to a rise in mitochondrial Cyt Ox activity. Two positive relationships were found: 1) between type I MHC and VO2tot increments (r = 0.65, P < 0.05), 2) between training volumes and VO2tot increments (r = 0.53, P < 0.05; N = 23). The training program produced an 8.2% significant increase in type I MHC (P < 0.05) while type II MHC decrease was not significant (-4.4%). Although they were almost non-existent before the program, muscle fibers which co-expressed type I and II MHC displayed a marked increase afterwards (4.9 +/- 5.7 vs 1.1 +/- 2.1%, P < 0.05). Muscle GSH-Px activity, at rest, did not respond to endurance training or Se supplementation. The results suggest that the neuromuscular system is still in an evolutive state after 10 weeks of endurance training, and that selenium supplementation has no effect on endurance training-induced adaptations.
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PMID:Effects of endurance training on skeletal muscle oxidative capacities with and without selenium supplementation. 917 70


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