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)

The effects of moderate alcohol intake on serum (SHEX)- and urinary beta-hexosaminidase (UHEX) were studied in ten healthy volunteers, who ingested 60 g of 100% ethanol daily for 10 days. The drinking period was preceded and followed by an abstinence period. Moderate drinking and abstinence were rapidly and significantly reflected on SHEX, while UHEX levels did not change significantly during the study. Gramma-glutamyl transpeptidase (GGT), aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) decreased during the first abstinence period (P less than 0.05), but stayed thereafter at a constant level. It is concluded that SHEX may better reflect recent alcohol consumption than UHEX, GGT, ASAT or ALAT.
Drug Alcohol Depend 1990 Feb
PMID:The effects of moderate drinking and abstinence on serum and urinary beta-hexosaminidase levels. 196 91

Rats intoxicated with ethanol at the dose of 0.6 g/100 g of the body weight during 4 weeks were fed on standard diet and the one containing 0.125, 0.25 and 0.5% L-cysteine. Intoxication of rats fed standard food causes an increase in the activity of cathepsin D and gamma-glutamyl-transpeptidase in the liver and an increase in the activity of alanine aminotransferase and gamma-glutamyl-transpeptidase in the blood serum. Consuming by rats food containing small and medium quantity of cysteine causes normalization of the activity of all enzymes, whereas consuming food containing large quantity of cysteine does not give such effect.
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PMID:[Effect of cysteine on protein metabolism in the liver of rats with ethanol-induced liver damage]. 198 88

Fatty liver can be determined by chronic abuse of alcohol, by means of direct action of the same on the level of membrane's proteins. The UDPG restores the levels of a membrane's component, the phosphoribosylpyrophosphate (PRPP), which normally results reduced in cellular cultures of rat's liver, after the addition of alcohol. It has been made a study on 40 patients (27 men and 13 women age medium 54 years) alcoholics for at least 1 year with a quantity of ethanol ingested less than 1 g gamma/die/kg of body weight with alternated values of serum GOT, GPT and gamma-GT and clinical aspects of a modest alcoholic hepatopathy, assigning through, at random in double blind, two groups of treatment: the first one with UDPG (400 mg/im/die for 30 days) the second one with placebo. It has been considered like variable of therapeutic effect the difference between basal value and the result at the end of treatment of these serum enzymes, it has been applied the Student's t test for the evaluation of the difference between treatments. It has been shown in the groups of patients analyzed with UDPG (not the group of placebo) reduction extremely significant for the gamma-GT (p = 0.00032) and GOT (p = 0.0138). In 5 treated cases, after an hepatic ultrasound imaging of comparison, at the end of the treatment, it has been demonstrated an apparent improvement of thickening of the echos; only 3/40 of the patients have certainly stopped to ingest alcoholic drinks.
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PMID:[Uridine diphosphate glucose (UDPG) in the treatment of hepatic disease from chronic alcohol abuse]. 208 Mar 8

Serum activities of alanine-aminotransferase (ALAT, EC 2.6.1.2), aspartate-aminotransferase (ASAT, EC 2.6.1.1), lactate dehydrogenase (LDH, EC 1.1.1.27), and alkaline phosphatase (AP, EC 3.1.3.1) were increased significantly after a dose of 0.16 g/kg/b. w. (ip.) carbon tetrachloride (tetrachloromethane) in rats pretreated with 10% (v/v) ethanol for one and 10 weeks in comparison with water/carbon tetrachloride-treated animals. At the end of 30 and 52 weeks of ethanol consumption these levels were very slightly increased or not detectable. Ethanol treatment alone did not cause an increase in serum enzyme activities or histological liver damage, but caused a diminished intake of fluid and food and in some cases also a reduction of weight gain in the animal body. Significant decrease in body weight after carbon tetrachloride was more evident in rats pretreated with ethanol (1 week greater than 10 greater than or equal to 52 weeks) than in water drinking animals, the lethality caused by carbon tetrachloride was also higher after one and 10 weeks than after 30 to 52 weeks of ethanol pretreatment. The results indicate a decrease of carbon tetrachloride toxicity with increased duration of ethanol pretreatment. This phenomenon could be attributed to reduced sensibility to those alcohol effects which are responsible for increase of carbon tetrachloride toxicity.
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PMID:Influence of ethanol pretreatment of differing duration on toxic effects of carbon tetrachloride in rats. 208 Sep 8

Cocaine has been associated with hepatotoxicities in man and is a potent hepatotoxin in mice. The theorized toxic metabolite of cocaine is thought to be generated by a multistep pathway mediated primarily by cytochrome P-450. Ethanol, whether administered acutely or chronically, is known to have diverse effects on numerous hepatocellular biochemical pathways. The present study was designed to characterize not only the effects of acute and chronic ethanol on cocaine-mediated hepatotoxicity but also on the hepatic reduced glutathione (GSH) in an attempt to correlate depletions of GSH with changes in toxicity. Male and female mice were administered an acute 50 mg/kg dose of cocaine either 1 hr after an acute 3 g/kg dose of ethanol, or after 5 days of consuming an ethanol-containing liquid diet. Serum alanine aminotransferase (ALT) activity was measured in blood collected 24 hr after the acute cocaine dose. In addition, hepatic reduced glutathione (GSH) and cytochrome P-450 content were measured at the point in the pretreatment where cocaine was administered. The results of this study indicate that both acute and chronic ethanol pretreatment can markedly enhance the hepatotoxicity of cocaine in both male and female mice and that the enhancement is significantly greater after chronic ethanol pretreatment. Hepatic GSH was slightly decreased 1 hr after an acute dose of ethanol and significantly decreased after chronic ethanol consumption.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res 1990 Feb
PMID:Potentiation of cocaine-mediated hepatotoxicity by acute and chronic ethanol. 217 68

In muscles preserved in formalin enzymes were not found to be active. In muscles treated by ethanol the ESD, GLO, GPT and PGP enzymes were active. The best results were obtained in the case of acetone treatment. The phenotypes ESD, GLO, GPT and PGP in tissues corresponded with the ones in the comparative blood samples.
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PMID:Polymorphism of isoenzymes in preserved muscle tissues. 221 May 47

To investigate the effect of cocaine on standard liver function tests (LFT), we studied 46 cocaine users with no history of parenteral drug use or homosexuality. LFT were similar in 21 users of cocaine only (Group A) and 25 users of cocaine and alcohol (Group B). Only three patients, two of whom were hepatitis B carriers, had an alanine aminotransferase level more than five units above normal limits. Group B patients were significantly more likely to complain of headaches, irritability, and loss of memory. We conclude that (1) non-parenteral cocaine use is rarely associated with significant LFT abnormalities and (2) alcohol may potentiate some adverse effects of cocaine.
Drug Alcohol Depend 1990 Oct
PMID:Liver function tests in non-parenteral cocaine users. 224 18

Various aliphatic alcohols potentiate the toxicity of a wide range of xenobiotics including several haloalkanes. The present series of experiments were designed to test: (i) whether a single subtoxic dose of alcohol can potentiate CCl4 and CHCl3 hepatoxicity, and (ii) whether this potentiation leads to greater animal lethality. Selected members of a homologous series of straight chain alcohols were chosen for this study. Methanol, ethanol, isopropanol, t-butanol, pentanol, hexanol, octanol, decanol, and eicosanol at equimolar doses (10 mmol/kg) were tested in the present investigation. Each alcohol was administered orally to male Sprague-Dawley rats (175-250 g) 18 hr prior to a single oral administration of CCl4 or CHCl3. Liver injury was assessed by plasma transaminases (alanine aminotransferase, ALT; aspartate aminotransferase, AST) and histopathological examination of liver sections 24 hr after the halomethane treatment. None of these alcohols alone increased plasma ALT or AST significantly, whereas CCl4 or CHCl3 administration to alcohol-treated animals resulted in significant elevation of plasma transaminases. Eicosanol (20-carbon alcohol) did not potentiate the toxicity of either halomethane. Methanol, ethanol, isopropanol, and decanol in combination with CCl4 caused massive liver damage but failed to augment CCl4 lethality. t-Butanol, pentanol, hexanol, and octanol significantly decreased the LD50 of CCl4. The hepatotoxic effects of CHCl3 were potentiated by all of the alcohols and the LD50s were also decreased significantly. On a comparative basis, alcohol-potentiated CHCl3 toxicity was greater than the toxicity of CCl4. These findings indicate that even though halomethane liver injury might be potentiated by alcohols, the underlying mechanisms differ among alcohols since not all alcohols potentiate the lethal effects of these halomethanes.
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PMID:Potentiation of CCl4 and CHCl3 hepatotoxicity and lethality by various alcohols. 225 8

The present investigation examines the possibility that Cd and ethanol have a significant toxicological interaction. This examination was warranted as exposure to either chemical is known to compromise human health. Inasmuch as both chemicals affect the morphology, biochemistry, and physiology of liver, it seemed reasonable to consider liver as a possible site of interaction. Specifically, the hypothesis that ethanol alters the hepatotoxic action of Cd was evaluated. Accordingly, male rats were injected iv with hepatotoxic (3.0 mg/kg) or lethal (4.5 mg/kg) dosages of Cd, 24 hr after single-dose ethanol administration (7 g/kg, po). Cd-induced hepatotoxicity was assessed by measuring the activities of alanine aminotransferase, aspartate aminotransferase, and sorbitol dehydrogenase in serum collected 10 hr after Cd injection. Lethality was assessed by recording the number of survivors over a 7-day period. Prior exposure to ethanol substantially reduced the lethal and hepatotoxic properties of Cd. Two mechanisms were evaluated in an effort to explain ethanol-induced suppression of Cd hepatotoxicity. Ethanol pretreatment was postulated to: (1) enhance Cd excretion in bile thereby decreasing hepatic Cd content and/or (2) reduce the interaction between Cd and target sites in liver such as organelles and cytosolic high-molecular-weight (HMW) proteins. The first proposed mechanism was incorrect as the biliary excretion of Cd was nearly abolished and the concentration of Cd in whole liver increased (33%) as a result of ethanol exposure. The second proposed mechanism was a plausible explanation of ethanol-induced suppression of Cd hepatotoxicity because ethanol pretreatment decreased (approximately 60%) the content of Cd in nuclei, mitochondria, and endoplasmic reticulum, and nearly eliminated the association of Cd with cytosolic HMW proteins. Reduction in the concentration of Cd in potential target sites of intoxication was caused by a metallothionein-promoted sequestration of Cd in cytosol.
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PMID:Ethanol decreases cadmium hepatotoxicity in rats: possible role of hepatic metallothionein induction. 226 92

In 1214 adult persons, the relationship between alcohol consumption, the "liver enzymes" and other metabolic parameters, including the serum lipids, were investigated. In 798 of the persons, glucose tolerance tests with measurement of plasma insulin were performed (young and old male and female adults, either volunteers or patients without liver-related diseases). There was a high correlation of the three transferases GOT, GPT and GGT not only with the reported alcohol consumption but also with the plasma insulin. Most of the insulin increase, however, occurred in that range of the three transferases which, so far, has erroneously been considered to be the normal one. The C-peptide showed the same behaviour. Plasma insulin was also raised in relation to overweight, but only in persons with the sum of the three transferases over 30 U/l, not in persons who did not drink alcohol and who had really normal transferases (sum of the three transferases below 30 U/l measured at 25 degrees C). The quotient of plasma insulin divided by the relative body weight (Broca Index) was constantly low in the range of really normal transferases (up to 30 U/l), thereafter rising significantly, but only in the range of the transferases so far erroneously considered to be the normal one (GOT to 17, GPT to 22, GGT to 28 U/l, thus sum up to 67). Serum glucose in the tolerance test also rose with the transferases but much less than the plasma insulin. The correlation between both GGT and the sum of the three transferases with the plasma insulin was significantly positive and independent of the relative body weight. It is concluded that overweight (which is generally believed to be the main risk factor for non-insulin-dependent diabetes), and insulin resistance (which leads to hyperinsulinaemia), are largely caused by the toxic effects of "normal" daily alcohol, more in the human male than in the female. Hyperinsulinaemia (which blocks lipolysis) is caused by a toxic effect of ethanol and its metabolites, independent of caloric input and overweight. Hyperinsulinaemia is at least in the human male at present, probably the most important cause of obesity. In obesity, caused by "normal" alcohol consumption, a vicious circle occurs: the enhancement of the triglycerides and, consequently, the free fatty acids leads to a further decrease of glucose utilization by the muscle. A continuously high glucose level has toxic effects: eventually the beta cells of the pancreas are exhausted.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The main cause of diabetes (type II): "normal" alcohol drinking]. 227 72


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