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)

Oral administration of a 50% ethanol extract of Abrus precatorius seeds (250 mg/kg) in albino rats for 30 and 60 days induced an absolute infertility in males which was reversible. Suppression of sperm motility in the cauda epididymis was the most pronounced effect of the treatment. Such treatment may affect the oxidative/energy metabolism of the cauda epididymis. Histological and histocytometric observations in testis and parareproductive tissues appeared normal while the protein, sialic acid, acid phosphatase and succinic dehydrogenase levels were significantly depleted.
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PMID:Post-testicular antifertility effects of Abrus precatorius seed extract in albino rats. 232 8

The present experiments were designed to study the effect of chronic ethanol consumption on endotoxin toxicity. The intravenous injection of endotoxin produced a more pronounced increase of serum AST and ALT activities in chronic ethanol-fed rats, when compared to controls. The activities of hepatic mitochondrial enzymes, succinate dehydrogenase and cytochrome oxidase, were also distinctly decreased by endotoxin treatment in chronic ethanol-fed rats. Consistent with these biochemical alterations, light and electron microscopic examinations revealed severe liver injury after endotoxin injection in chronic ethanol-fed rats. Furthermore, the increase of blood BUN and creatinine levels accompanied by the degeneration of the renal tubulus and slight infiltration of neutrophils into the glomerule were produced by endotoxin treatment and were more conspicuous in chronic ethanol-fed rats than controls. Therefore, the biochemical and histological evidence indicates that endotoxin markedly potentiates organ injury after chronic ethanol consumption. In addition, a more pronounced decrease in blood antithrombin III activity accompanied by an increase in fibrin degradation product level in blood was recognized in chronic ethanol-fed rats receiving endotoxin, when compared to controls receiving endotoxin. This increase of blood fibrin degradation product level correlated well with the decrease of antithrombin III activity (r = -0.6116; p less than 0.005). These findings of blood antithrombin III activity and fibrin degradation product level indicate that the coagulation-fibrinolysis system is more activated by endotoxin treatment after chronic ethanol consumption. Furthermore, the activation of the coagulation-fibrinolysis system was well correlated with biochemical and histological alterations representing hepatorenal involvement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endotoxin-induced hypercoagulability: a possible aggravating factor of alcoholic liver disease. 254 Oct 59

The biochemical consequences of moderate chronic ethanol ingestion has been scarcely investigated in spite of the fact that most of the human population drinks ethanol on a moderate basis. This paper describes some metabolic effects produced by moderate ethanol consumption. The substitution of drinking water in rats for a 10% ethanol solution during 4 weeks resulted in: a) a decrease of blood urea and citrulline synthesis in liver mitochondria; b) a slight inhibition in state 3 and state 4 respiration either with glutamate-malate as substrates or succinate as substrate; c) no change in ADP/O ratio with succinate but slight increase with glutamate-malate; d) a reduction of the cytochrome oxidase activity and cytochromes a+a3 content; e) a 42% increase in the succinate dehydrogenase activity and a small but constant increase in the Vmax (no change in the Km) of the adenine nucleotide translocase activity in liver mitochondria. These results show that even moderate, but continuous ethanol ingestion, produces metabolic responses that must be carefully evaluated to define health risk in larger human groups.
Alcohol
PMID:Effects of moderate chronic ethanol consumption on rat liver mitochondrial functions. 254 37

To determine if impaired intestinal absorption contributes to the folate deficiency observed in chronic alcoholics, we assessed in vivo folate absorption in Hanford mini-pigs fed ethanol with an adequate diet. Sixteen minipigs were pair-fed diets supplemented with ethanol or sucrose to 60% of total calories for 11 mo. In the ethanol-fed pigs peak blood alcohol concentrations averaged 28 mmol/L, serum alanine transaminase and aspartate transaminase activities were elevated, and liver histology showed a centrilobular distribution of succinate dehydrogenase. Tissue folate concentrations were comparable in both groups. The jejunal uptake of folic acid, measured by intestinal perfusion, was similar in both groups of animals and was not affected by acute exposure to 445 mmol/L ethanol. The in vivo hydrolysis of polyglutamyl folate was reduced by 35% in one ethanol-fed minipig. Decreased hydrolysis of polyglutamyl folate may represent an early step in the development of folate deficiency in chronic alcoholics.
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PMID:Folate absorption in alcoholic pigs: in vivo intestinal perfusion studies. 259 32

The effect was studied of chronic alcohol intake in the rat during pregnancy and lactation on the brown adipose tissue (BAT) in pups. The idea was to find a possible relationship to cot death since in some cot death victims increased amounts of BAT have been observed. Exposure to ethanol increased the relative weight of the brown adipose tissue in pups and enhanced both its total protein content and the activities of the oxidative enzymes, succinate dehydrogenase and cytochrome oxidase. In the BAT of pups sympathetic activity, as demonstrated by noradrenaline, was also increased by long-term exposure to alcohol. In theory, an increased thermogenic capacity of the BAT in the newborn together with other factors such as emotional stress and infections could lead to death from hyperthermia, in which case only non-specific morphological signs would be found in the cadaver.
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PMID:Foetal and lactational exposure to alcohol increases oxidative capacity of brown adipose tissue in the rat. A possible relationship to cot death. 260 16

The present study was carried out to elucidate the effect of long-term alcohol intake on the oxidative capacity of brown adipose tissue in the rat. Rats housed at room temperature were given water containing 10% ethanol for six months, while controls received water alone. Fully cold-acclimated rats (exposed to +4 degrees C for 6 weeks) served as the second control group. Alcohol did not alter the food intake of the rats compared with the controls kept at room temperature, but it did cause a mean decrease of 8 ml in fluid consumption. There was no difference in the increase in body weight between the groups housed at room temperature. Body weight of the rats exposed to cold did not change during cold acclimation. No morphological liver changes were observed in alcohol-fed rats, but some changes related to long-term alcohol consumption were found in the myocardium. Chronic alcohol intake increased the quantity of brown adipose tissue and its protein content but changes were not as great as in the cold-acclimated rats nor did alcohol increase protein content per unit of the adipose tissue as did cold. On the other hand, the specific activity of mitochondrial cytochrome oxidase increased by 90% and that of succinate dehydrogenase by 130% in alcohol-fed rats, whereas specific activities of these enzymes displayed little or no change in the cold-acclimated rats. Results suggest that chronic alcohol ingestion induces the oxidative capacity of the interscapular brown adipose tissue in the rat, increasing the mass of BAT and specific activities of mitochondrial enzymes.
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PMID:Chronic alcohol intake induces the oxidative capacity of brown adipose tissue in the rat. 283 55

Mitochondrial enzymes and respiration were studied in the hearts of mice exposed to ethanol in utero from gestational Day 8 to parturition. This treatment had previously been shown by electron microscopy to result in myofibril loss and mitochondrial abnormalities. Ethanol was administered to pregnant mice by a liquid diet paradigm and pair-fed dams were used as controls. Ethanol exposure in utero reduced the activities of two mitochondrial inner membrane enzymes, cytochrome c oxidase and succinate dehydrogenase, in the hearts of perinatal mice. Secondly, mitochondrial respiration under both State 3 and 4 conditions with a NAD-linked substrate was depressed in the hearts obtained from the ethanol-exposed fetal mice. However, when a flavin-linked substrate was used, State 3 (ADP-stimulated) but not State 4 respiration was depressed. This study illustrates that in utero exposure to ethanol is deleterious to the functioning of cardiac mitochondria in newborn mice, which in turn could contribute to the development of the heart pathologies present in the Fetal Alcohol Syndrome.
Alcohol Clin Exp Res 1988 Apr
PMID:Cardiac mitochondrial abnormalities in a mouse model of the fetal alcohol syndrome. 289 3

1. A reduction in the dietary concentration of choline, an essential nutrient for Drosophila melanogaster, from the optimal concentration of 80 micrograms/ml of defined medium to 8 micrograms/ml diminished the level of tissue phosphatidylcholine to less than one-third the normal level in third instar larvae without significantly altering the amount of phosphatidylethanolamine. 2. The rates of synthesis of phospholipids, triglycerides, diglycerides and monoglycerides were reduced by the choline-deficiency, and the chain length of fatty acids in lipids was shortened. 3. The activity of succinic dehydrogenase, a mitochondrial enzyme, was decreased by the deficiency, but the activities of fumarase, sn-glycerol-3-phosphate dehydrogenase, alcohol dehydrogenase, sn-glycerol-3-phosphate oxidase and fatty acid synthetase were unaffected. A choline-deficiency did not alter the ultrastructure of mitochondria of larval fat body cells. 4. Choline-deficient individuals were more susceptible to the toxic effects of ethanol during larval and pupal development, and less adept at utilizing ethanol as a substrate for adult tissue synthesis.
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PMID:The effects of a choline deficiency on the lipid composition and ethanol tolerance of Drosophila melanogaster. 290 4

1. The succinate dehydrogenase (SDH) and D-3-hydroxybutyrate dehydrogenase (HBDH) activities were measured over a 24-hr period in rat liver mitochondria after chronic alcohol ingestion and withdrawal. 2. The diurnal patterns of both the enzyme activities were shown to change after alcohol consumption, with 64-66% decrease in the daily mean levels. 3. The diurnal rhythms of the SDH and HBDH activities are partially restored 24-72 hr after alcohol withdrawal. 4. There was no correlation between changes in both the enzyme activities and the NAD+/NADH ratio of liver mitochondria from control, ethanol-fed and withdrawn rats over the day.
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PMID:Diurnal changes in succinate and D-3-hydroxybutyrate dehydrogenase activities of rat liver mitochondria after chronic alcohol consumption and withdrawal. 290 76

The work deals with the effect of carbon sources, presence of protein synthesis inhibitors (cycloheximide and chloramphenicol) and dehydration regime on the enzyme activity of the dried yeast Saccharomyces cerevisiae. The yeast grown on molasses and dried by aeration demonstrated a notable increase of the NADH-dehydrogenase and succinate dehydrogenase activities as compared with the analogously treated yeast grown on ethanol. The latter showed a notable rise only in the activity of NADH-dehydrogenase during slow drying. Addition of protein synthesis inhibitors into the cultivation medium caused no decrease of activities of the above mentioned enzymes of the dried yeasts in any variant under study.
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PMID:[Effect of protein synthesis inhibitors on the activity of mitochondrial enzymes of Saccharomyces cerevisiae during desiccation]. 332 Oct 29


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