Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a five-week feeding trial, 90 broiler chicks were used to study the response of serum and liver alanine aminotransferase (ALT) aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH) and alkaline phosphatase following the replacement of varying levels (0, 20, 40, 60, 80 and 100 per cent) of fishmeal protein by soyabean meal protein. The results showed that both serum ALT and AST activities increased significantly (P less than 0.01) with the increasing levels of substitution of soyabean meal for fishmeal. Regression analysis showed a significant (P less than 0.01) positive correlation between ALT and AST activities and the level of soyabean meal substitution with correlation coefficient, r, of 0.93 and 0.98, respectively. The liver ALT and AST tended to increase with the increasing proportion of soyabean meal although such increases were not significant (P greater than 0.01). Serum and liver SDH and alkaline phosphatase activities were not significantly influenced by diet.
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PMID:Dietary fishmeal versus soyabean meal: an assessment of serum and liver enzyme response in the chicken. 235 76

Serum activity of alanine aminotransferase (ALT) was consistently increased in dogs with canine X-linked muscular dystrophy (CXMD), a primary myopathy characterized by profound and on-going skeletal muscle necrosis. In order to determine whether the ALT was of liver origin, serum activity of creatine kinase (CK), aspartate aminotransferase (AST), ALT, and sorbitol dehydrogenase (SDH) obtained from dystrophic dogs was compared with enzyme activity present in clinically normal dogs. In dystrophic dogs at all ages tested, serum activity of CK, AST, and ALT was increased, and significant increases were present in dogs four weeks or older. In contrast, SDH activity in dystrophic dogs was not statistically different from values in clinically normal dogs. Ultrastructural examination of liver tissue revealed no evidence of hepatic degeneration in dystrophic dogs. It was concluded that increased serum activity of ALT in the dog may be associated with severe skeletal muscle degeneration, without concurrent hepatocellular necrosis.
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PMID:Increased serum alanine aminotransferase activity associated with muscle necrosis in the dog. 236 22

Mercuric chloride was administered once i.p. to female Fischer-344 rats at doses of 0, 0.2, 0.6 and 1.8 mg/kg. Although there were no alterations in the urinary excretion of lactate dehydrogenase, significant elevations in the activities of urinary (U) alkaline phosphatase, glutamic-pyruvic transaminase (GPT) and glutamic-oxalacetic transaminase (GOT) indicated that mercuric chloride was nephrotoxic. There was no evidence of hepatotoxicity as hepatic glucose-6-phosphatase and serum sorbitol dehydrogenase were essentially unaffected by mercuric chloride administration. The activities of ethylmorphine demethylase, hexobarbital oxidase and aldrin epoxidase determined in vitro were not inhibited by mercuric chloride although aniline hydroxylase activity was decreased. Of the four phase-II reactions measured, only the glucuronidation of chloramphenicol was diminished by treatment with mercuric chloride. Results from the in vivo studies on the metabolism of lindane, which indicated no change in the excretion of free or conjugated metabolites, were in close agreement with the in vitro data suggesting that the nephrotoxic effects of mercuric chloride do not alter the urinary excretion of the model substrate lindane.
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PMID:A comparison of in vitro and in vivo methods for evaluating alterations in hepatic drug metabolism following mercuric chloride administration. 242 44

Elevated levels of serum enzymes are frequently associated not only with alcohol-related organ damage but also with excessive alcohol consumption and alcoholism without significant tissue injury. However, both in the early detection of alcoholism as well as also in the diagnosis of alcohol-related diseases the sensitivities and specificities of these enzyme markers vary considerably. They may be influenced by nonalcohol-related diseases, enzyme-inducing drugs, nutritional factors, metabolic disorders, age, smoking, etc. Consequently, we have neither a single laboratory test--enzyme marker--nor a test combination that is reliable enough for the exact diagnosis between alcohol- and nonalcohol-related organ damage. In most cases it is possible to determine the tissue from which the elevated enzyme is derived, but only occasionally enzyme changes reflect the quantity of the tissue injury. Gamma-glutamyltransferase (GGT) is the most widely used laboratory marker of alcoholism and heavy drinking, detecting 34-85% of problem drinkers and alcoholics. However, the unspecificity of increased serum GGT limits its use for general screening purposes. Its value in the follow-up of various treatment programs, however, is well established. An elevated level of serum aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) in an alcoholic or a heavy consumer indicates alcohol-induced organ damage. The use of test combinations significantly improves the information received with single serum enzyme determinations. An ASAT/ALAT ratio greater than 1.5 can be considered as highly suggestive for the alcoholic etiology of the liver injury. Still better discrimination between alcoholic and nonalcoholic origin of the liver disease may be achieved by the determination of the ratio of GGT to alkaline phosphatase. If this ratio exceeds 1.4 the specificity of the finding in favor for alcoholic liver injury is 78%. The determination of the mitochondrial isoenzyme of ASAT also improves the diagnostic value of ASAT determination. The ratio of mitochondrial isoenzyme to total over 4 is highly suggestive for alcohol-related liver injury. In general, however, the determination of serum activities of other enzymes such as ornithine carbamyl transferase, lactate dehydrogenase, isocitrate dehydrogenase, sorbitol dehydrogenase, alcohol dehydrogenase, guanase, aldolase, alkaline phosphatase or glutathione S-transferase do not significantly improve the diagnostic information obtained with more conventional laboratory markers of liver injury.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of enzymes for the diagnosis of alcohol-related organ damage. 243 6

The suitability of DL-alpha-lipoic acid (LA) to serve as an antidote in cadmium (Cd) toxicity in rat hepatocytes was investigated. Isolated hepatocytes were exposed to 200 and 450 microM Cd in the presence of 0.2, 1.0 and 5.0 mM LA, respectively. After 30 min of incubation various criteria of cell viability were monitored. Lipoic acid markedly diminished Cd uptake. Concomitantly, Cd-induced membrane injury, as reflected by the leakage of aspartate aminotransferase and sorbitol dehydrogenase (SDH) was decreased. Moreover, LA protected against intracellular toxic responses to Cd, such as a decrease in cellular SDH activity, a decrease in cellular acid soluble thiols, especially in total glutathione, a decrease in cellular urea and an increase in thiobarbituric acid (TBA) reactants, as a measure of lipid peroxidation. Most protective effects were seen in hepatocytes challenged with the lower Cd concentration and coincubated with 5 mM LA. In contrast, at 450 microM Cd even the highest LA concentration applied either did only reverse Cd-effects incompletely (SDH-response, TBA-reactants) or did not protect at all (Cd uptake, enzyme leakage, loss of glutathione). The data indicate that DL-alpha-lipoic acid serves as a protective tool against Cd-induced membrane damage and cell dysfunction in hepatocytes. This stands as long as Cd exposure is low enough to permit interaction with LA prior to interaction with cell structures.
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PMID:Protective effects of DL-alpha-lipoic acid on cadmium-induced deterioration of rat hepatocytes. 250 68

Twenty-eight Norwegian Red Cattle dairy cows were fed silage ad libitum and restricted amounts of concentrates. Blood samples were collected before morning feeding, once or twice weekly, from 2 weeks before to 12 weeks after calving. Parameters of liver function, carbohydrate status and fertility were recorded in order to assess their interrelationships. Eight cows were treated for clinical ketosis. Four of these had to be treated 2 or 3 times. Aspartate aminotransferase and bilirubin showed the highest within-animal coefficients of correlation with acetoacetate. Analysis of variance revealed a significant effect of carbohydrate status (indicated by plasma acetoacetate levels) on the levels of aspartate aminotransferase, glutamate dehydrogenase and sorbitol dehydrogenase, though only a small part of the total variation was explained by this factor. The estimated volume density of liver fat in the 4th week of lactation averaged 6.0 +/- 6.4% (+/- SD) ranging from 0.1-25.1%. Liver fat content at this stage of lactation was not significantly correlated with other indicators of liver function or carbohydrate status. Cows treated for clinical ketosis had significantly lower plasma progesterone values at the time of first ketosis treatment than untreated multiparous cows. The frequency of high progesterone values (greater than 3 ng/ml) being significantly lower in treated than in untreated cows during the period from 3-5 weeks post partum, though not at later stages. In conclusion, the results revealed a significant relationship between carbohydrate status and liver function, and also between clinical ketosis and luteal function.
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PMID:Variations in parameters of liver function and plasma progesterone related to underfeeding and ketosis in a dairy herd. 259 86

This investigation was undertaken to assess the potential of ingested 1,2-dibromo-3-chloropropane (DBCP) to cause testicular and hepatorenal injury, in light of the paucity of data applicable to risk assessment of DBCP in drinking water. Adult male Sprague-Dawley rats were supplied ad libitum with water containing 0, 5, 50, 100, and 200 ppm DBCP for 64 days. A dose-related decrease in water consumption occurred during the study. The 200-ppm animals drank less than half as much water as controls, consumed less food, and subsequently exhibited significantly lower body weight gain. DBCP ingestion thus was not directly proportional to the level of chemical in the water, although daily and cumulative intake of DCP were concentration dependent. Average daily intake of DBCP for the 64-day exposure period was as follows: 5 ppm = 0.4 mg/kg/day; 50 ppm = 3.3 mg/kg/day; 100 ppm = 5.4 mg/kg/day; 200 ppm = 9.7 mg/kg/day. Blood samples were taken after 2, 4, and 6 weeks of exposure and at the terminal sacrifice and assayed for serum glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, sorbitol dehydrogenase, and ornithine-carbamyl transferase activities and BUN levels. No evidence of liver damage at any exposure level was indicated by either the clinical chemistry indices or histopathology. Histologic examination revealed an apparent increase in the number of nuclei per renal proximal tubule cross-section in the 200-ppm group, possibly indicative of an increased turnover of proximal tubular cells. A slight, but statistically significant, decrease in absolute testicular weight was manifest in the 200-ppm animals, although the decrease was not significant when testicular weight was calculated as g/100 g body wt. Epididymal sperm counts and serum luteinizing hormone, follicle stimulating hormone, and intratesticular testosterone levels were not altered by any dose of DBCP. A qualitative histopathological examination of the testicular seminiferous epithelium failed to reveal any abnormalities in the spermatogenic process.
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PMID:Assessment in rats of the gonadotoxic and hepatorenal toxic potential of dibromochloropropane (DBCP) in drinking water. 262 Jul 97

It is well established that caloric restriction extends life span and significantly retards the rate of occurrence of most age-associated degenerative disease processes. A paucity of data exists relative to the mechanisms by which caloric restriction accomplishes these events. We have examined the effect of caloric restriction in rats on several hepatic enzymes of intermediary metabolism. The activities of glycolytic and supporting enzymes including lactate dehydrogenase, pyruvate kinase, sorbitol dehydrogenase, and alcohol dehydrogenase were all decreased in response to caloric restriction. Fructose 1-phosphate aldolase and creatine phosphokinase were not altered. Likewise, enzymes associated with lipid metabolism (malic enzyme and glycerokinase) were reduced (fatty acid synthetase was reduced, but not to a statistically significant degree). Activities of enzymes supporting gluconeogenesis (glutamate oxaloacetate transaminase, tyrosine aminotransferase, glutamate pyruvate transaminase, glutamate dehydrogenase, amino acid oxidase, malate dehydrogenase, and glucose 6-phosphatase) were either unchanged or increased significantly by caloric restriction. Glucagon levels were decreased. Comparisons between young ad libitum fed and older calorically restricted rats revealed similar but not identical metabolic activity. These results suggest that caloric restriction produces an effect on intermediary metabolism, favoring the role of glucagon and glucose synthesis; but limiting the role of insulin and glucose catabolism in the liver. The former observation provides for the efficient support of peripheral tissues and the latter a level of energy production necessary only for self maintenance. Limited lipid metabolism suggests decreased potential for fatty acid epoxide formation and free radical damage to cellular macromolecules. Additionally, caloric restriction may delay the progressive age associated changes in the activities of some of the enzymes investigated.
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PMID:Effect of chronic caloric restriction on hepatic enzymes of intermediary metabolism in the male Fischer 344 rat. 266 33

The hepatotoxic and mutagenic potentials of 2-nitropropane, nitromethane, and nitroethane were compared. Hepatotoxicity was assessed biochemically and histopathologically in BALB/c mice. In male mice, plasma activities of the hepatic enzymes sorbitol dehydrogenase, alanine aminotransferase, and aspartate aminotransferase were significantly elevated 48, 72, and 96 hr after ip administration of 9 mmol/kg 2-nitropropane, but not at 24 hr and not after administration of smaller doses of 2-nitropropane nor after nitromethane or nitroethane (9 mmol/kg). In female mice a dose of 6.7 mmol/kg of 2-nitropropane was sufficient to cause hepatotoxicity. The histopathological evaluation supported the biochemical results, and livers of mice that had received 2-nitropropane (9 mmol/kg) showed damage, particularly in the periportal region. Mutagenicity was tested in Salmonella typhimurium tester strains TA98, TA100, and TA102. Both 2-nitropropane and its anionic form, propane-2-nitronate, were mutagenic but the nitronate was the more powerful mutagen. Nitromethane, nitroethane, nor their nitronates caused an increase in the number of revertant colonies over those seen in control plates. The results suggest that the primary nitroalkanes are much less hepatotoxic and mutagenic than 2-nitropropane.
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PMID:Comparison of the hepatotoxicity in mice and the mutagenicity of three nitroalkanes. 267 74

Seven horses were given 0.5 mg of carbon tetrachloride/kg of body weight via a nasogastric tube. Subsequent hepatocellular damage was monitored by serum enzyme determinations of sorbitol dehydrogenase, isoenzyme 5 of lactate dehydrogenase, and aspartate transaminase activities. Creatinine kinase activity was evaluated as an indicator of muscle cell damage. Sorbitol dehydrogenase, isoenzyme 5 of lactate dehydrogenase, and aspartate transaminase activities were significantly (P less than 0.05) increased by 24 hours after carbon tetrachloride administration. Isoenzyme 5 of lactate dehydrogenase and sorbitol dehydrogenase activities returned to baseline several days before aspartate transaminase activity returned to baseline. Creatine kinase activity remained unchanged.
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PMID:Variations in serum sorbitol dehydrogenase, aspartate transaminase, and isoenzyme 5 of lactate dehydrogenase activities in horses given carbon tetrachloride. 272 9


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