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)

In order to establish evidence of serum enzyme activities in toxicological long-term experiments alterations of alanine aminotransferase (ALAT) and aspartate aminotransferase (ASAT) in the serum of rats were investigated after subchronic ethanol pretreatment and following trichloroethylene exposure. Somewhat lower enzyme activities were found in ethanol treated animals than in those who only got water in nearly all cases. Significant ALAT and ASAT decreases occurred after giving higher ethanol concentrations (5% and 10%, v/v) for 30 weeks. It is possible that this fact among other things could be responsible for the only slight enzyme elevations after trichloroethylene in long-term ethanol pretreated rats.
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PMID:Serum enzymes in toxicity of trichloroethylene after subchronic ethanol pretreatment. 386 70

Ethanol metabolism in rat hepatocytes isolated either from the periportal (pp) or the perivenous (pv) area by collagenase gradient perfusion was compared to reveal metabolic factors that could be associated with the development of perivenous alcoholic liver damage. Cells were also isolated from rats given ethanol (E) chronically by addition to the drinking fluid. One group (EM) received in addition the alcohol dehydrogenase inhibitor 4-methylpyrazole, which potentiated the ethanol treatment by causing sustained elevated diurnal blood ethanol levels. Fatty degeneration ensued in only one-third of the E rats but in all of the EM rats. The periportal/perivenous activity distributions of alanine aminotransferase (ALAT) and glutamate dehydrogenase (GLDH) were 2.2 and 0.75, respectively. Both ethanol treatments significantly decreased the ALAT and increased the GLDH activities, but did not change their pp/pv distributions. Ethanol treatment also increased ethanol and acetaldehyde oxidation, but to the same extent in pp and pv cells. The increase was more marked in cells from EM rats despite their more severe liver fatty degeneration. Ethanol incubation also increased the lactate/pyruvate ratio to the same extent in pp and pv cells both from control or ethanol-treated rats. Our results indicate that periportal and perivenous hepatocytes convert ethanol via acetaldehyde to acetate equally well and with similar effects even after chronic ethanol treatment. Consequently, preferential damage of the perivenous area after chronic ethanol intake is not caused by inherent or acquired differences in ethanol metabolism between perivenous and periportal hepatocytes. Rather, sinusoidal gradients only established in the intact liver may exaggerate the metabolic imbalance by ethanol in the perivenous area, thus explaining its greater vulnerability to damage by alcohol abuse.
Alcohol Clin Exp Res
PMID:Comparison of ethanol metabolism in isolated periportal or perivenous hepatocytes: effects of chronic ethanol treatment. 390

Weanling, male Sprague-Dawley rats given 10% ethanol in the drinking water and food ad lib. for up to 8 weeks consumed 17% of their calories as ethanol. The alanine aminotransferase (ALT), aspartate aminotransferase (AST), and liver histology by light microscopy were unaffected by this treatment. Similarly, hepatic microsomal NADPH-cytochrome c reductase, ethylmorphine N-demethylase and benzphetamine N-demethylase activities were also not affected by ethanol consumption. On the other hand, cytochrome P-450 content, aniline hydroxylase activity and acetaminophen metabolism as measured by both the cysteine conjugate and the [3H]acetaminophen covalently-bound to microsomal protein were increased significantly by ethanol consumption. The maximal effect was seen by 6 weeks. The 2- to 3-fold increase in aniline and acetaminophen metabolism, the absence of liver damage, and the similarity in weight gains and caloric intakes for controls and treated animals suggest that the rat on 10% ethanol in the drinking water is a reasonable model for studies of the effect of moderate alcohol consumption on specific biochemical pathways.
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PMID:Studies on the effect of chronic consumption of moderate amounts of ethanol on male rat hepatic microsomal drug-metabolizing activity. 393 44

The level of alanine aminotransferase (ALT) in blood donors has been related to the frequency of posttransfusion hepatitis in recipients. Sixty-seven donors with elevated ALT levels were evaluated to define the duration and significance of the elevation. The ALT level remained elevated in 41 donors (61%) for a mean interval of 9 months. The ALT level was greater than the aspartate aminotransferase in all of the donors. Alcohol intake did not correlate with ALT level. Donors with persistently elevated ALT levels had a significantly higher mean percent ideal body weight (128 +/- 3.9) than donors whose ALT level became normal (116 +/- 3.1). Nine donors with elevated ALT levels for at least 6 months had needle biopsies of the liver. Seven had prominent fatty vacuolization of hepatocytes without evidence of alcoholic hepatitis. One biopsy demonstrated chronic persistent hepatitis. No other cause for the elevated ALT levels could be identified. An overweight male donor with an isolated ALT elevation may need no further investigation unless clinical evaluation suggests a source of liver injury.
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PMID:The persistence and significance of elevated alanine aminotransferase levels in blood donors. 398 3

The association between a number of blood and serum quantities and industrial organic solvent exposure and poisoning, alcohol consumption, smoking, and age was analysed in 277 subjects by multiple regression analysis. Solvent poisoning was associated with changes in S-creatine kinase concentrate at the P less than 0.001 level (higher if exposed, lower if non-exposed at the examination time). Solvent exposure seemed to potentiate the effects of smoking on B-hemoglobin conc. and B-erythrocyte volume fraction, and the effect of age on S-creatinine conc. at the P less than 0.05 level, while there was no interaction between alcohol consumption and solvents. Alcohol consumption in itself, as well as smoking and age, were highly significantly associated with changes in a large number of blood and serum quantities. There was no difference in the alcohol markers (mean erythrocyte volume = MCV, S-alanine aminotransferase and S-urate) in patients with solvent poisoning compared to healthy volunteers. The results indicate that studies on the effects of solvents of haematology and biochemistry are not valid unless the effects of alcohol, smoking and age are established; and that excessive alcohol consumption is an unlikely explanation for the symptoms of patients with solvent poisoning. The findings suggest that smoking and age may have combined effects with solvents.
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PMID:Influence of solvents, alcohol, smoking and age on biological tests. 398 56

Renal arterial embolization is often used in the treatment of patients with renal cell carcinoma, either preoperatively to facilitate nephrectomy or as palliative therapy in advanced cases. Eighteen patients (18/58; 31%) underwent renal arterial embolization in our department since 1979, initial 10 cases with Gelfoam and steel coil (group G) and recent 8 cases with absolute ethanol (group A). Clinical studies of daily changes of symptoms and blood chemistry in both groups after embolization were compared and the results were as follows: Severe flank pain was noted immediately after embolization but thereafter well controlled without analgesics in group A. The patients in group G experienced no pain during the procedure of embolization but have had moderate flank pain of two or three days' duration with nausea and/or vomiting and required surgical procedure within a few days after embolization. Post embolization fever in group A was described as higher than that in group G significantly. Leukocytosis was noted to be persistent for up to seven days and blood chemistry showed transient marked elevations of GOT, GPT and LDH immediately after the procedure without significant value in both groups. Embolization to advanced tumor with many parasitic vessels or massive local invasion may not always be available for remaining of viable-appearing tumor cells in venous lumen, as if palliative treatment. Absolute ethanol may be more useful as the embolizing substance than Gelfoam and steel coil by reason of producing wide severe infarction of diseased kidney. Broad marked infarction due to renal arterial embolization may make pathological diagnosis difficult. Immunological effects of renal arterial embolization were not observed in short term patients survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal arterial embolization for renal cell carcinoma]. 402 78

The perfusion in situ of the rat liver reveals appearance of enzymes of different subcellular localization, potassium ions and lipid components in the perfusate. Ethanol introduction at different doses induces the most expressed changes in the activity of catalase, lactate dehydrogenase, arginase and alanine aminotransferase and in the potassium removal from hepatocytes. A degree of the evoked changes depends on the dose.
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PMID:[Effect of different doses of ethanol on the release of enzymes and lipids from the perfused rat liver]. 403

The effects of bromobenzene, carbon tetrachloride, and N-nitrosodimethylamine (DMN) on hepatic glutathione S-transferase activity were studied in untreated and in phenobarbital- or ethanol-treated rats. In phenobarbital-treated rats, the isozymic composition of the hepatic cytosolic glutathione S-transferases was changed after giving hepatotoxic chemicals; glutathione S-transferases 2-2(AA), 3-3(A), 1-2(B), 3-4(C), and 4-4 + 5-5(D + E) were present in cytosol from control rats, but only glutathione S-transferases cochromatographing with transferases 4-4 + 5-5(D + E) were detected in rats given carbon tetrachloride or bromobenzene. A marked decrease in hepatic and an increase in serum glutathione S-transferase activity were also observed after carbon tetrachloride or bromobenzene treatment, but little change was seen after giving DMN. On the contrary, in untreated or ethanol-treated rats, DMN administration decreased hepatic glutathione S-transferase activity and caused an elevation in serum glutathione S-transferase activity. The isozymic composition of the hepatic cytosolic glutathione S-transferases after giving DMN to untreated rats was also altered, but the alteration was much less than that observed after giving carbon tetrachloride or bromobenzene to phenobarbital-treated rats. The elevation in serum glutathione S-transferase activity was accompanied by an increase in both serum glutamate-pyruvate transaminase activity and serum bilirubin concentrations. Thus, hepatic glutathione S-transferase activity was altered and released into serum after giving hepatotoxic chemicals, and the alteration in glutathione S-transferase activity was dependent on treatment with phenobarbital or ethanol.
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PMID:Alteration of hepatic glutathione S-transferases and release into serum after treatment with bromobenzene, carbon tetrachloride, or N-nitrosodimethylamine. 407 84

Carbon tetrachloride (CCl4)-induced hepatotoxicity was potentiated by pretreatment with beta-phenethyl alcohol, abundantly present in sake. The injury was determined by serum GPT levels and histological examination. Similar results were observed in ethanol- and phenobarbital-pretreated rats. Acetaminophen-induced hepatotoxicity was not accentuated by beta-phenethyl alcohol or ethanol pretreatment. The activities of liver microsomal enzymes, such as cytochrome P-450, cytochrome b5 reductase, aniline hydroxylase and aminopyrine demethylase, were not altered in beta-phenethyl alcohol-pretreated rats. Thus, CCl4-induced hepatotoxicity potentiation by beta-phenethyl alcohol administration is postulated to be due to a mechanism other than increased free radical generation.
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PMID:Potentiation of carbon tetrachloride hepatotoxicity by beta-phenethyl alcohol. 608 1

The effect of ethanol on the activity of ornithine decarboxylase (ODC), tyrosine aminotransferase (TAT), alanine aminotransferase (ALAT) and lactate dehydrogenase (LD), as well as on protein concentration, was studied in regenerating rat liver after partial hepatectomy. It was found that administration of an ethanol-containing liquid diet for 5 days after partial hepatectomy caused a significant accumulation of proteins in the liver. The activities of ODC and TAT were stimulated by ethanol treatment in the beginning of the regeneration. In control livers, partial hepatectomy decreased the activity of ALAT, but ethanol prevented this decrease. No differences in the activity of LD was found between ethanol and control groups after partial hepatectomy. When the half-lives of ODC and TAT were measured 24 hr after partial hepatectomy by using cycloheximide, it appeared that ethanol caused a significant stabilization of both enzymes. It is concluded that ethanol caused inhibition of degradation of ODC and TAT and it is suggested that this could be a general phenomenon, and could markedly contribute to the pathological accumulation of proteins in the liver after chronic ethanol consumption.
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PMID:Inhibition of protein degradation in regenerating rat liver by ethanol treatment. 611 5


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