Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have made a comparison between groups of rats fed ethanol and a diet that received intragastric infusion of ethanol continuously for prolonged periods varying only in the amount of fat in the diet (percentage of total calories as fat was 5, 25, and 35%). A fourth group of rats fed high fat (32% of calories) and a diet marginal in protein, vitamins and minerals was also studied. Control rats were pair-fed dextrose in isocaloric amounts. For rats fed diets containing 5, 25, 32, and 35% fat, the average blood alcohol levels achieved were 216, 224, 266 and 353 mg/100 ml, respectively. Average weight gains of the ethanol fed rats were: 15.4, 19.6, 14.7, and 14.9 g/week, respectively. Serum alanine aminotransferase (ALT) levels of the ethanol-fed rats averaged 123, 292, 144, and 213 units/liter, respectively. ALT levels in pair-fed controls for the rats fed 32% fat averaged 62 and those of chow-fed controls averaged 49 units/liter. Comparison of liver biopsy-semiquantified morphological findings revealed an increased 3-4+ fatty change in the ethanol-fed rats also fed the high fat rats. Moreover, fibrosis was only observed centrilobularly in rats fed diets with varying fat content (5, 25, 32, or 35% of calories): 0/16, 10/17, 4/6, and 3/7 rats, respectively, over a 5-mon period of feeding. Electron microscopy showed that ito cells predominated in the scarred areas. The mechanism for the centrilobular necrosis-fibrosis was investigated in rats given a diet of ethanol plus 32% fat diet by measuring the level of adenine nucleotide in repeated liver biopsies in five pair of rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res 1986
PMID:Ethanol-induced hepatic fibrosis in the rat: role of the amount of dietary fat. 354 25

Ethanol at initial concentrations between 0.75 and 6 g/l produced a dose-dependent release of the enzymes glutamic-pyruvic-transaminase and sorbitol dehydrogenase (GPT, SDH) from the isolated perfused rat liver. At the concentration of 6 g/l, it also decreased the oxygen consumption and elevated the calcium content of the isolated livers. These toxic effects of ethanol were significantly enhanced in livers, the glutathione content of which had been depleted by pretreatment with phorone. Ethanol-induced toxicity in glutathione-depleted isolated livers could be prevented both by inhibition of alcohol dehydrogenase with 4-methylpyrazole and of xanthine oxidase with allopurinol. In rats, in vivo, 1.6 g/kg ethanol injected intravenously produced a small increase in serum GPT and SDH concentrations 4 h after its administration. This increase in enzyme activities was several-fold higher and longer lasting in rats pretreated with phorone. Glutathione depletion per se did not induce hepatotoxicity in vitro or in vivo. Since glutathione is involved in several lines of defense against oxidative damage, our results of an enhanced susceptibility of glutathione-depleted livers to ethanol toxicity favour the hypothesis that ethanol exerts its hepatotoxic action via an activation of molecular oxygen.
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PMID:Enhancement by glutathione depletion of ethanol-induced acute hepatotoxicity in vitro and in vivo. 360 86

Lyophilised ethanol and aqueous extracts of Rosmarinus officinalis young sprouts and total plant have been evaluated for choleretic and hepatoprotective activities in the rat. R. officinalis ethanol extracts prepared from young sprouts show a significant dose-related choleretic activity and are more active than the total plant extract. Aqueous extracts of young sprouts show a significant hepatoprotective effect on plasma GPT levels when given as pretreatment before carbon tetrachloride intoxication while the whole plant extract was inactive. Both sprouts and whole plant aqueous extracts were ineffective when given after carbon tetrachloride administration.
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PMID:Comparative choleretic and hepatoprotective properties of young sprouts and total plant extracts of Rosmarinus officinalis in rats. 361 6

The effects of acute administration of ethanol and nicotine either singly or in combination, have been studied on the plasma amino acids levels and certain biochemical and hematological parameters in the rats. Both ethanol and its combination with nicotine produced significant reduction in the levels of a number of amino acids and the total amino acid pool. Only the levels of taurine and hydroxyproline were increased in the ethanol treated rats, whereas its combination with nicotine resulted in markedly elevated levels of hydroxyproline, ornithine and taurine. These changes were also accompanied by a significant rise in blood glucose, ALT, AST, blood urea and uric acid and a significant reduction in the total protein and triglycerides levels. Nicotine by itself produced less profound effect on the plasma amino acids and other biochemical parameters.
Alcohol Drug Res 1987
PMID:Studies on ethanol and/or nicotine induced acute changes in the levels of plasma amino acids and other biochemical parameters of male Wistar rats. 362 13

Since ethanol consumption decreases hepatic aminotransferase activities in vivo, mechanisms of ethanol-mediated transaminase inhibition were explored in vitro using mitochondria-depleted rat liver homogenates. When homogenates were incubated at 37 degrees with 50 mM ethanol for 1 hr, alanine aminotransferase decreased by 20%, while aspartate aminotransferase was unchanged. After 2 hr, aspartate aminotransferase decreased by 20% and by 3 hr, alanine and aspartate aminotransferases were decreased by 31 and 23%, respectively. Levels of acetaldehyde generated during ethanol oxidation were 525 +/- 47 microM at 1 hr, 855 +/- 14 microM at 2 hr, and 1293 +/- 140 microM at 3 hr. Although inhibition of alcohol oxidation with methylpyrazole or cyanide markedly decreased ethanol-mediated transaminase inhibition, neither incubation with acetate nor generation of reducing equivalents by oxidation of lactate, malate, xylitol, or sorbitol altered the activity of either enzyme. However, semicarbazide, an aldehyde scavenger, prevented inhibition of both aminotransferases by ethanol. Moreover, incubation with 5 mM acetaldehyde for 1 hr inhibited alanine and aspartate aminotransferases by 36 and 26%, respectively. Cyanamide, an aldehyde dehydrogenase inhibitor, had little effect on ethanol-mediated transaminase inhibition. Thus, metabolism of ethanol by rat liver homogenates produces transaminase inhibition similar to that described in vivo and this effect requires acetaldehyde generation but not acetaldehyde oxidation. Since addition of pyridoxal 5'-phosphate to assay mixes did not reverse ethanol effects, aminotransferase inhibition does not result from displacement of vitamin B6 coenzymes.
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PMID:Evidence for the generation of transaminase inhibitor(s) during ethanol metabolism by rat liver homogenates: a potential mechanism for alcohol toxicity. 366 1

A study was carried out to confirm the pathogenetic role of ethanol in the development of chronic active hepatitis (CAH) and to assess if previous or current superimposed hepatitis B virus (HBV) infection could be relevant to the course of alcoholic liver disease (ALD). We examined clinical and laboratory reports of 57 alcoholics with biopsy-proven CAH. Serum and/or tissue HBV markers and the presence or absence of cirrhosis were investigated. Alcohol was the only aetiological factor present in a small group of CAH, with or without histological findings suggestive of alcoholic damage. Age, sex and survival were similar among the subgroups of CAH with and without previous or current HBV infection and among the subgroups of CAH with and without associated histological alcoholic features. Among the laboratory data, the AST/ALT ratio was higher in CAH without previous or current HBV infection. The mean age was comparable in CAH patients with and without cirrhosis, whereas the cumulative 5-year survival was worse in CAH with cirrhosis (87% vs. 49%). These data suggest a difference in alcohol susceptibility in our subjects.
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PMID:Features of chronic hepatitis in alcoholics. A survey in Milan. 369 15

Protection against the toxic effects of chronic alcohol consumption was observed in male guinea pigs maintained on a high-ascorbic-acid diet (vitamin C-deficient chow plus 2.0 mg ascorbic acid/ml drinking water) as compared to animals on a low-ascorbic-acid diet (vitamin C-deficient chow and from 0.025 to 0.050 mg ascorbic acid/ml drinking water). Alcohol was orally administered to the guinea pigs at a dose of 2.5 g/kg for up to 14 weeks. Levels of serum aspartate aminotransferase and serum alanine aminotransferase were significantly elevated in animals on the low-ascorbic-acid diet that received alcohol, 120 and 250%, respectively. In contrast, in animals on the high-ascorbic-acid diet that received alcohol, levels of alanine aminotransferase were not significantly elevated and levels of aspartate aminotransferase were elevated 50%. In addition, some of the animals on the low-ascorbic-acid diet that received alcohol for 12 to 14 weeks developed hepatic steatosis and necrosis, whereas none of the animals on the high-ascorbic-acid diet that received alcohol for the same length of time manifested these changes.
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PMID:Ascorbic acid chronic alcohol consumption in the guinea pig. 371 80

Pharmacological investigations were carried out to evaluate the hepatoprotective effects of Crepis rueppellii and Anisotes trisulcus. Ethanolic extracts of these plants were investigated for their ability to reduce mortality of mice after ethanol intoxication and to lower the activities of plasma glutamic-pyruvic transaminase (GPT) after carbon tetrachloride-induced hepatitis in rats. Crepis and Anisotes extracts and a 50:50 mixture of both at 200 mg/kg presented significant hepatoprotective effects in both experimental situations. The traditional therapeutic indications of these plants have been largely confirmed.
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PMID:Hepatoprotective properties of Crepis rueppellii and Anisotes trisulcus: two traditional medicinal plants of Yemen. 374 59

After 7 weeks on a vitamin E deficient diet plasma and liver content of vitamin E were reduced by 60-70%. This treatment, a two week chronic ethanol intake or their combination all caused a significantly higher level of liver glutathione as compared to untreated rats. The chronic ethanol treatment also increased the activity of both alcohol dehydrogenase and aldehyde dehydrogenase and this effect was potentiated by vitamin E deficiency. The activity of the mitochondrial enzyme glutamate dehydrogenase was reduced both by vitamin E deficiency and by ethanol treatment. The activity of the cytosolic alanine aminotransferase was, on the other hand, markedly elevated by vitamin E deficiency, but this effect was completely abolished by ethanol treatment. Several similarities between the effects of chronic ethanol intake and vitamin E deficiency indicates that a poor vitamin E status may potentiate some of the ethanol-induced derangements in the liver.
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PMID:Combined vitamin E deficiency and ethanol pretreatment: liver glutathione and enzyme changes. 378 47

Urinary excretion of salsolinol (6,7-dihydroxy-1-methyl-1,2,3,4-tetrahydroisoquinoline) in 30 male alcoholic patients during the withdrawal period was determined. They were divided into two groups, i.e., Group A with 14 subjects had a high level of urinary salsolinol (51.9 +/- 40.8 ng/mg creatinine) on admission to a hospital, and Group B with 16 subjects showed a low level of the substance (3.9 +/- 1.9 ng/mg creatinine). Following a sustained drinking bout, urinary salsolinol in Group A declined to a normal level within a few days. We found that the subjects in Group A showed a greater excretion of urinary dopamine and norepinephrine than those in Group B. There were no differences between the two groups in levels of blood ethanol, serum GOT, GPT and gamma-GTP.
Alcohol
PMID:Individual difference in urinary excretion of salsolinol in alcoholic patients. 381 48


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