Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:[Morphologic indices the influence of selenium and vitamin E on the course of experimental myocardial infarct]. 101 63

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)
 ...
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.
 ...
PMID:Vitamin E deficiency as a model of precocious brain aging: assessment by X-ray microanalysis and morphometry. 855 24

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.
 ...
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

Mercury intoxication has been associated with male reproductive toxicity in experimental animals and mercury may have the potential to produce adverse effects on fertility in men. Vitamin E may protect against toxic effects of mercury in the liver and other tissues. To investigate the protective role of vitamin E against mercuric chloride toxicity for the testis, epididymis, and vas deferens of adult male mice, animals were treated with either mercuric chloride 1.25 mg/kg/day, vitamin E 2 mg/kg/kg, or a combination of the two treatments. Control animals were treated with water. Treatments were administered by daily gavage for 45 days. An additional group of animals treated with mercuric chloride were permitted to recover for 45 days after mercuric chloride treatments. Parameters studied included serum testosterone, epididymal sperm count, motility, and morphology, epididymal and vas deferens adenosine triphosphatase (ATPase), phosphorylase, sialic acid, glycogen and protein, testicular succinate dehydrogenase (SDH), phosphatases, cholesterol, ascorbic acid, and glutathione. Fertility was evaluated by sperm positive vaginal smears after overnight cohabitation with a female. Mercuric chloride produced a reduction in epididymal sperm count, sperm motility, and sperm viability, and there were no sperm-positive smears in this group. Biochemical tests from the male reproductive organs were also altered by mercuric chloride treatment. Coadministration of vitamin E with mercuric chloride prevented the changes in sperm and biochemical parameters and was associated with control rates of sperm positive smears after cohabitation. Animals given vitamin E with mercuric chloride also had lower concentrations of mercury in the testis, epididimyis, and vas deferens. Permitting animals to recover for 45 days after mercuric chloride treatment resulted in partial recovery of sperm and biochemical parameters. Vitamin E cotreatment has a protective role against mercury-induced male reproductive toxicity.
 ...
PMID:Protective effect of vitamin E against mercuric chloride reproductive toxicity in male mice. 1173 24

In the present study an attempt has been made to evaluate the effect of Tiron along with Zinc, Selenium and Vitamin E against vanadium intoxication in female albino rats. Toxicant caused significant increase in the activities of serum transaminases, serum alkaline phosphatase and lactate dehydrogenase. Significant decrease was observed in blood sugar, serum albumin and triglyceride levels whereas serum proteins, cholesterol and urea levels increased significantly during toxicity (p </= 0.001). Hepatic lipid peroxidation increased significantly, whereas significant depletion was observed in reduced glutathione after vanadium administration. The activity of glucose-6-phosphatase in the liver was also inhibited significantly after vanadium administration. A significant rise was observed in glycogen content of liver and kidney after toxicant exposure. Activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase were inhibited significantly on the contrary activity of acid phosphatase elevated in kidney. Histopathological examination of the liver and kidney using light and ultramicroscopic study also substantiated the above findings. It was found that therapy with Tiron was effective but significant recovery in all the parameters was found with Tiron + Se followed by Tiron+ VitE and Tiron +Zn.
 ...
PMID:Effect of tiron and its combination with nutritional supplements against vanadium intoxication in female albino rats. 1753 42

The present study has been designed to explore the nitric oxide mechanism in the protective effect of desipramine, venlafaxine and trazodone against I/R induced oxidative stress and mitochondrial dysfunction in mice. Vitamin E was taken as standard antioxidant. Laca mice (25-30 g) were subjected to twice BCCAO occlusion (5 min) at the interval of 10 min, followed by 96 h reperfusion. The drug treatments were started from the day of surgery and continued for the next four days. After 96 h the animals were sacrificed for biochemical (malondialdehyde, nitrite concentration, superoxidedismutase, catalase, redox ratio and GST) and mitochondrial enzyme complex (NADH dehydrogenase, succinate dehydrogenase, MTT assay and cytochrome c oxidase) estimations. Ischemia caused significant oxidative damage and mitochondrial enzyme dysfunction after 96 h of reperfusion as compared to sham operated animals. Antidepressant (desipramine, venlafaxine and trazodone) treatment significantly attenuated oxidative damage and restored mitochondrial enzyme complex activities as compared to control (I/R) group. Further, protective effects of desipramine (15 mg/kg) and/or venlafaxine (5 mg/kg) were attenuated by l-arginine (100 mg/kg) or sildenafil (5 mg/kg) pretreatment. Further, L-NAME (10 mg/kg) or 7-NI (10 mg/kg) pretreatment with desipramine (15 mg/kg) and/or venlafaxine (5 mg/kg) significantly potentiated their protective effect which was significant as compared to their effect alone. The present study highlights the involvement of nitric oxide mechanism in the protective effects of desipramine and venlafaxine against I/R induced oxidative stress and mitochondrial dysfunction in mice.
 ...
PMID:Protective effect of desipramine, venlafaxine and trazodone against experimental animal model of transient global ischemia: possible involvement of NO-cGMP pathway. 2062 74