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)

The activity of the mitochondria internal membrane ensymes alpha-ketoglutarate dehydrogenase and succinate dehydrogenase was studied after rats poisoning with CCl4. It is established that the activity of these enzymes lowers considerably under effect of CCl4, which is more pronounced for alpha-ketoglutarate dehydrogenase. The pretreatment of animals with inducer of microsomal oxidases intensifies the damaging effect of CCl4 on the internal membranes of mitochondria and decreases the LD50 value for CCL4. Administration of actinomycin D simultaneously with polycyclic hydrocarbons prevents intensification of the CCl4 hepatotoxic effect caused by 3-methylcholanthrene and dibenz (a, h) anthracene.
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PMID:[Effect of tetrachloromethane on alpha-ketoglutarate dehydrogenase and succinate dehydrogenase activity in mitochondria of rat liver under conditions of administration of polycyclic hydrocarbons]. 89 14

A hepatic stimulator substance (HSS) was extracted from the liver of male weanling SD rats according to the method of LaBrecque. The mice were injected with carbon tetrachloride or D-galactosamine to induce hepatic injuries and the protective effect of HSS on thus induced hepatic damage was investigated. The results were as follows: (1) HSS could suppresses the elevation of sGPT and sGOT induced by carbon tetrachloride intoxication in a dose-dependent manner. (2) Hepatic histological findings indicated that the degree of CCl4 or D-galactosamine-induced hepatic lesions could be lessened by HSS. (3) CCl4-induced reduction of hepatic mitochondrial succinic dehydrogenase activity could be restored by HSS. (4) Insulin-glucagon enhanced the survival of D-galactosamine intoxicated mice and stimulated hepatocyte proliferation, thus showing less pronounced hepatic damage.
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PMID:[Protective effect of hepatic stimulator substance against experimental acute liver failure in mice]. 179 5

A single intraperitoneal injection of hepatocarcinogen diethylnitrosamine induced emergence of a new subpopulation of "small" hepatocytes (64-128 mkm2), disappearing by the 30th day after carcinogen injection. But 5 injections of the tumor promotor phenobarbital 7 days after carcinogen treatment prolonged the existence of such "small" hepatocytes up to 3 months. The quantitative cytochemical measurement of succinic dehydrogenase activity (respiratory enzyme of mitochondria) showed these cells to be resistant to cytotoxic action of CCl4. These data are consistent with the earlier reported results obtained in analogous experiments with 4-dimethylaminoazobenzene and phenobarbital.
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PMID:[Detection of cells resistant to the cytotoxic action of CCl4 in rat hepatocyte populations following a single exposure to diethylnitrosamine and subsequent injections of phenobarbital]. 377 59

It is found that hepatic cells of intact rats measuring 129-192 mcm2 are resistant to cytotoxical action of carbon tetrachloride (CCl4). After a single interperitoneal injection of the carcinogen 4-dimethylaminoazobenzene, small hepatocytes (64-128 mcm2) appear to be maintained for one month following five injections of phenobarbital. These small hepatocytes are resistant to cytotoxical action of CCl4. The resistance was studied using a cytochemical test on succinate dehydrogenase. A direct dependence exists between the cell size and the sensitivity to CCl4 among large sized hepatocytes.
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PMID:[Detection of cells resistant to the cytotoxic action of CCl4 in the hepatocyte populations of rats following a single exposure to 4-dimethylaminoazobenzene combined with subsequent injections of the tumor promoter phenobarbital]. 393 6

The ATPase activity (proton ATPase) of rat liver mitochondria was studied 2, 24, 28, 96 and 168 h after acute tetrachloromethane poisoning. It is established that the tetrachloromethane poisoning. It is established that the tetrachloromethane poisoning is accompanied by a considerable activation of mitochondrial H+-ATPase and a decrease of the DNP and Ca+, Na+ and K+ activating influence on it. Maximum changes in the H+-ATPase activity is observed 24 h after poisoning. Changes in the H+-ATPase properties are accompanied by a fall in the alpha-ketoglutarate dehydrogenase and succinate dehydrogenase activities and by disturbance of the liver mitochondria contractile properties. The electrochemical membrane potential of the mitochondria under the effect of tetrachloromethane is supposed to be reduced due to a primary damage of the phospholipid matrix of the coupling membrane and an increase in its proton conductivity.
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PMID:[ATPase activity of rat liver mitochondria in acute tetrachloromethane poisoning]. 646 Mar 65

The effect of carrot extract on carbon tetrachloride (CCl4)-induced acute liver damage was evaluated. The increased serum enzyme levels (viz., glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, alkaline phosphatase, sorbitol and glutamate dehydrogenase) by CCl4-induction were significantly lowered due to pretreatment with the extract. The extract also decreased the elevated serum bilirubin and urea content due to CCl4 administration. Increased activities of hepatic 5'-nucleotidase, acid phosphatase, acid ribonuclease and decreased levels of succinic dehydrogenase, glucose-6-phosphatase and cytochrome P-450 produced by CCl4 were reversed by the extract in a dose-responsive way. Results of this study revealed that carrot could afford a significant protective action in the alleviation of CCl4-induced hepatocellular injury.
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PMID:Hepatoprotective activity of carrot (Daucus carota L.) against carbon tetrachloride intoxication in mouse liver. 750 Jun 38

The hepatoprotective effect of the ethanol/water (1:1) extract of Eclipta alba (Ea) has been studied at subcellular levels in rats against CCl4-induced hepatotoxicity. Ea significantly counteracted CCl4-induced inhibition of the hepatic microsomal drug metabolising enzyme amidopyrine N-demethylase and membrane bound glucose 6-phosphatase, but failed to reverse the very high degree of inhibition of another drug metabolising enzyme aniline hydroxylase. The loss of hepatic lysosomal acid phosphatase and alkaline phosphatase by CCl4 was significantly restored by Ea. Its effect on mitochondrial succinate dehydrogenase and adenosine 5'-triphosphatase was not significant. The study shows that hepatoprotective activity of Ea is by regulating the levels of hepatic microsomal drug metabolising enzymes.
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PMID:Hepatoprotective effects of Eclipta alba on subcellular levels in rats. 814 70

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

The potential sensitivity of liver specific protein regucalcin as a biochemical marker of chronic liver injury with carbon tetrachloride (CCl4) administration in rats was investigated. CCl4 (10%; 1.0 ml/100 g body wt) was orally given 5 times at 3-day intervals to rats, and the animals were killed by bleeding at 3, 6, 18, and 30 days after the first administration of CCl4. The body weight of rats was significantly lowered 3 and 6 days after CCI4 administration as compared with that of control rats administered with corn oil, and then the weight was restored at 18 and 30 days. Serum glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) activities were significantly increased 3 days after the administration, while a significant increase in serum y-glutamyltranspeptidase (gamma-GTP) activity was seen at 3 and 6 days after the administration. Serum GOT, GPT, and gamma-GTP activities were restored to control levels at 18 and 30 days after CCl4 administration. Serum albumin, alpha-fetoprotein, and ammonium levels were not changed by CCl4 administration. Meanwhile, serum regucalcin concentration was markedly increased 3 and 6 days after CCl4 administration, and a significant increase in serum regucalcin concentration was observed 18 and 30 days after the administration. Liver regucalcin mRNA and liver cytosolic regucalcin levels were significantly decreased 18 and 30 days after CCl4 administration. Liver content of calcium, which intracellular calcium homeostasis is maintained, was significantly increased between 3 and 30 days after CCl4 administration. Hepatic mitochondrial succinate dehydrogenase activity was significantly increased 30 days after the administration. The present study demonstrates that serum regucalcin has a potential sensitivity as a specific biochemical marker of chronic liver injury with CCl4 administration in rats.
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PMID:Potential role of regucalcin as a specific biochemical marker of chronic liver injury with carbon tetrachloride administration in rats. 1248 26

Propolis (bee glue), a resinous wax-like beehive product has been used since ancient times for its pharmaceutical properties. In the present study, the ethanolic extract of propolis (50, 100, 200 and 400 mg/kg, p.o.) was studied for its hepatoprotective activity against carbon tetrachloride (CCl4, 1.5 ml/kg, i.p.) induced liver damage in rats. Administration of CCl4 caused a sharp elevation in the activity of serum transaminases, serum alkaline phosphatase, acid phosphatase and hepatic lipid peroxidation (LPO) levels, and a significant decrease in the ATPase, alkaline phosphatase and succinic dehydrogenase activities in the liver and kidney and hepatic GSH level. The treatment with propolis extract at the doses of 200 and 400 mg/kg significantly reversed the various biochemical alterations in blood, liver and kidney induced by CCl4 intoxication. The hepatoprotective property of propolis may be due to its antioxidant activity.
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PMID:Evaluation of hepatoprotective potential of propolis extract in carbon tetrachloride induced liver injury in rats. 2392 41


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