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 different doses of chlorfenvinphos given in diets with low-protein and optimal-protein level to young Wistar rats of both sexes were, after 10 or 30 days, without the significant influence on the activity of several serum enzymes used as diagnostic markers in determining the liver damage or disease, as for example:sorbitol dehydrogenase, glutamic dehydrogenase, glucosephosphate isomerase (PHI), aspartate and alanine aminotransferase. Not even important changes were found in the activity of aromatic amino acids aminotransferases in the brain and in protein content in the brain and liver of rats fed diets contaminated with chlorfenvinphos, irrespective of the protein concentration in the diet. Only in some cases at the highest concentration of chlorfenvinphos in the diets the decreased activity of aromatic amino acids aminotransferases appeared in the liver, more evident in low-protein rats. The decrease of the PHI activity in the brain and the inhibition of acetylcholinesterase activity in the serum and brain depended mainly on the amount of chlorfenvinphos in the diets and to a lower degree on the amount of protein. All changes caused by chlorfenvinphos normalized during two weeks after its elimination from the diets.
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PMID:Alterations in some biochemical processes in the organism of rats being under the influence of chlorfenvinphos administered in diets with variable protein content. 648 45

Treatment of male and female rats with carbon tetrachloride (CCl4, twice weekly, 0.2 ml/kg p.o.) and a 5% alcohol solution during four weeks evoked strong increments of the serum enzyme activities of the aminotransferases (GOT, GPT) and the sorbitol dehydrogenase (SDH). These occurred earlier and were more pronounced in male compared to female rats. Hepatic triglyceride contents as a measure of fatty infiltration was augmented three-fold both in males and females at the end of the experiment. Hepatic hydroxyproline contents were enhanced seven-fold in males, but only two-fold in females. It is concluded that female rats are less susceptible to CCl4--alcohol-induced liver damage, especially hydroxyproline accumulation, which is explained by the known fact that females are more resistant against CCL4-hepatotoxicity as a consequence of a minor role of bioactivation in the metabolic degradation of CCL4 by females.
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PMID:Sex differences in the susceptibility of rats to carbon tetrachloride--alcohol-induced liver injury. 670 9

Cd has a strong affinity for sulfhydryl groups and is hepatotoxic. Thus, to further understand the mechanism of Cd-induced liver injury, the effect of increased and decreased hepatic glutathione (GSH) concentration on Cd-induced liver injury was examined. Liver GSH was lowered by pretreating rats with phorone (250 mg/kg, ip) or diethyl maleate (0.85 mg/kg, ip) 2 hr prior to challenge with various doses of Cd. Ten hours after Cd (1) 40-80% of the rats pretreated with phorone or diethyl maleate and challenged with 1.0-2.0 mg Cd/kg died whereas no mortality was observed in the control group; (2) plasma enzyme activities of alanine (ALT) and aspartate (AST) aminotransferase and sorbitol dehydrogenase (SDH) were markedly increased in phorone and diethyl maleate-pretreated rats challenged with Cd (0.7-2.0 mg/kg) versus control rats; and (3) moderate changes in liver histology were observed in corn oil pretreated and Cd challenged rats, while prior depletion of GSH potentiated histopathologic changes in liver produced by Cd alone. Another group of rats received cysteine (1.9 g/kg, po) 3 hr prior to injection of a lethal dose of Cd. Cysteine pretreatment increased liver GSH levels by 22% 3 hr after administration and attenuated Cd-induced liver injury as evidenced by marked decreases in plasma ALT, AST, and SDH activities. Pathological changes in liver were also reduced. These data indicate that liver reduced GSH concentration is important in modulating Cd-induced hepatotoxicity.
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PMID:Changes in hepatic glutathione concentration modify cadmium-induced hepatotoxicity. 671 May 2

Antitoxic properties of cobamamide, a coenzymic form of vitamin B12, were studied in experimental toxic hepatitis induced by CCl4. The data obtained as a result of the assessment of the bromosulfalene test and activity of sorbitol dehydrogenase and alanine aminotransferase point to a demonstrable hepatoprotective action of cobamamide. Normalization of the indicators studied evidences that the drug intensifies the recovery processes occurring in the liver of rabbits with toxic hepatitis.
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PMID:[Antitoxic action of cobamamide in experimental hepatitis]. 673 13

Studies by Liehr et al. suggest that endotoxins are important in the pathogenesis of galactosamine hepatitis (Gal-N hepatitis) in rats. Lactulose (9.1 gm per kg per day) prevents hepatic lesions induced by Gal-N; an antiendotoxin effect of lactulose is postulated. However, commercial preparations of lactulose are contaminated with galactose, which shows a competitive action to Gal-N. To analyze the effect of galactose, male Wistar rats were pretreated with lactulose (Duphalac, 9.1 gm per kg per day) and given Gal-N (375 mg per kg i.p.). After 24 hr, serum was analyzed for glutamic pyruvate transaminase, glutamate dehydrogenase, and sorbitol dehydrogenase activities. Pretreatment with Duphalac, even 1 hr before Gal-N, abolished toxicity. Duphalac contains 10 gm galactose per 100 ml. Galactose was given in a similar concentration and similar inhibition occurred. Pretreatment with purified lactulose (9.1 gm per kg for 5 days) diminished the effects of Gal-N but did not normalize enzyme concentrations. Because small doses of galactose (80 and 300 mg per kg) showed similar inhibitory effects, we conclude that the protective effect of commercial lactulose preparations is mainly due to galactose contamination and not to an antiendotoxin effect.
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PMID:Galactosamine hepatitis, endotoxemia, and lactulose. 683 15

Halothane hepatotoxicity was observed after exposing hyperthyroid rats to 0.625% halothane for 4 hr under hypoxic conditions (10% O2). In this model, increases in serum enzyme activities of the alanine aminotransferase (GPT) and the sorbitol dehydrogenase (SDH) were evident immediately following exposure and were six-fold higher than in the phenobarbital-hypoxic model. Plasma free-fluoride levels estimated immediately after exposure to halothane were increased twofold in halothane-exposed hyperthyroid rats under hypoxic conditions as were increased twofold in halothane-exposed hyperthyroid rats under hypoxic conditions as compared to a sixfold increase in the phenobarbital-hypoxic model. The concentration of glutathione in liver was more markedly decreased in hyperthyroid rats than in phenobarbital-induced rats. The fact that no clear-cut correlation was found between defluorination and hepatotoxicity in both models may favor the hypothesis that a non-defluorinated metabolite of halothane, e.g., 2-chloro-1,1,1-trifluoroethyl radical, is the reactive intermediate responsible for the liver lesions. On the other hand, intracellular hypoxia due to hypermetabolism during the hyperthyroid state may be the reason for the higher sensitivity of hyperthyroid rats.
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PMID:Halothane hepatotoxicity in hyperthyroid rats as compared to the phenobarbital-hypoxia model. 686 87

The activity of serum enzymes, such as, creatine kinase (CK), pyruvate kinase (PK), aldolase (ALD), lactate dehydrogenase (LDH), sorbitol dehydrogenase (SbDH), malate dehydrogenase (MDH), glutamate-aspartate aminotransferase (AST), glutamate-alanine aminotransferase (ALT), myokinase (MK), glucosephosphate isomerase (GPI), alkaline phosphatase (AlkP), pseudocholinesterase (PsCHE) isocitrate dehydrogenase and gamma-glutamyltranspeptidase (gamma-GTP), was determined in 256 patients with progressing myodystrophy (PMD) (Duchenne's form in 125, Becker's form in 14, pelvicohumeral form in 36, humeroscapulofacial form in 19, ocular form in 10, other rare forms in 34, and nonidentified forms in 13 patients). In the control group (64 men, 56 women and 50 children), the activity of the enzymes was found to depend on the patients' sex and age. With regard to both parameters, i. e. the degree of the enzyme activity rise and the frequency of the pathological values the most informative were CK, then PK and ALD, and then all the other enzymes. Of all the PMD forms the enzymatic activity appeared to be the highest in patients with the pseudohypertrophic malignant form. By determining the activity of five enzymes (CK, ALD, LDH, AST and ALT) and taking into consideration the patient's age, the onset and the duration of the disease one can distinguish between sick and healthy subjects, as well as between various forms of PMD.
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PMID:[Serum enzyme dynamics in progressive muscular dystrophies]. 703 17

The normal level of human serum alcohol dehydrogenase (EC 1.1.1.1) (ADH) activity which is not measurable by conventional methods was found to be within the range 0.07-0.56 U/1 when measured by a sensitive method based on a coenzyme recycling reaction. In different liver diseases the normal upper limit of serum ADH activity was found to be exceeded up to 70 times. Although ADH activity under pathological conditions usually parallels that of other enzymes, e.g., sorbitol dehydrogenase (EC 1.1.1.14) (SDH) and alanine transaminase (EC 2.6.1.2) (ALT), its relative elevation above the upper normal limit is generally greater, particularly in the early stages of viral hepatitis. Observations on some patients also suggested that very early stages of liver damage, caused by drugs or secondary malignancy, could be detected by increases of serum ADH activity when the activities of some other liver specific enzymes were still within their normal values. A pilot experiment on rats, intoxicated with carbon tetrachloride, showed that serum ADH activity could reflect acute liver parenchymal damage more sensitively than SDH and ALT activity.
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PMID:Serum alcohol dehydrogenase activity in liver diseases. 703 78

Female, male and castrated male ferrets were studied. Weight gain plateaued at 28 weeks of age with males about 500 g heavier than females. No statistically significant differences in haematology were observed with age, but alkaline phosphatase and alanine aminotransferase levels fell while glucose increased. Haemolysis led to various changes including marked increases in total protein, albumin, inorganic phosphate and sorbitol dehydrogenase.
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PMID:Haematological and serum chemistry profiles of ferrets (Mustela putorius furo). 707 59

Reference (normal) ranges for alkaline phosphatase, total bilirubin, urea nitrogen, chloride, cholesterol, total carbon dioxide, creatine phosphokinase, gamma glutamyl transpeptidase, glucose, lactic dehydrogenase, aspartate and aminotransferase, alanine aminotransferase, sorbitol dehydrogenase and triglycerides were established for cattle, sheep, pigs, ponies and ducks by use of the ABA-100 and A-Gent reagents (Abbott Laboratories). Most of the results agreed with those in the literature where methods were similar. Results were divided according to age for all species except ducks. Differences were noted between age groups with certain tests. The day-to-day reproducibility of control sera results are also presented.
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PMID:Clinical chemistry reference values of normal domestic animals in various age groups--as determined on the ABA-100. 714 Mar 2


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