Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of the red blood cell enzymes transketolase, glutathione reductase, and aspartate transaminase, and their activation by the coenzymes thiamine, riboflavin, and pyridoxine, the pyruvate tolerance test, the leucocyte vitamin C concentration, and the activity in serum of gamma-glutamyl transferase were measured in a series of 35 patients with alcohol-related illness. The incidence of thiamine deficiency was 31% as assessed by the activation of transketolase, and 55% as assessed by the pyruvate tolerance test. The incidence of riboflavin deficiency was 23% and of ascorbic acid deficiency 91%. No cases of pyridoxine deficiency were detected. The pyruvate tolerance test was found to be a more sensitive test of thiamine deficiency than the transketolase activation, and the activation of red blood cell aspartate transaminase was found to be a poor indicator of pyridoxine deficiency. There was a poor correlation of the gamma-glutamyl transferase activity with the degree of vitamin deficiency, suggesting that alcohol exposure is only partly responsible for the observed vitamin deficiency.
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PMID:Detection and incidence of B and C vitamin deficiency in alcohol-related illness. 3 28

Enzymic memory is a kinetic phenomenon observable in double displacement mechanisms. The defining feature of enzymic memory is the occurrence of different rates of transfer for a common transferable group from the substituted enzymes obtained with different donor substrates. Memory behavior was previously demonstrated for both the bovine and human liver rhodaneses (EC 2.8.1.1). Steady state kinetic tests for enzymic memory have now been done with ascorbate oxidase (EC 1.10.3.3) and aspartate aminotransferase (EC 2.6.1.1). The results were positive with ascorbate oxidase, which showed an oxygen reactivity ratio of 1:20:300 for the reduced enzymes obtained with reductate, araboascorbate, and ascorbate, respectively. Results were negative for the aminotransferase tested with the alternate donors glutamate and cysteine sulfinate, with oxaloacetate as the common acceptor. The structural basis of the ascorbate oxidase results was probed by comparison of both the ultraviolet absorption and fluorescence spectra of the oxidized enzyme with those of the reduced forms obtained with ascorbate and reductate. The results are consistent with a conformational basis for the memory phenomenon.
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PMID:Enzymic memory. Steady state kinetic and physical studies with ascorbate oxidase and aspartate aminotransferase. 47 84

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

Alcoholics admitted for detoxification were entered into a double blind placebo controlled trial of oral supplementation with an antioxidant cocktail (vitamin E, beta carotene, vitamin C and selenium) in order to determine the effect of this supplementation on the rate of resolution of a serum marker of free radical activity and abnormal serum biochemistry. The molar proportion of linoleic acid that was diene conjugated (a marker of free radical activity), was increased in the alcoholics 2.9% +/- 1.2 (mean +/- S.D.) compared to normal controls 1.3% +/- 0.6 (P < 0.0001) but fell at a similar rate during the first week of hospitalisation in supplemented and placebo-treated patients with a mean fall of 53.7% (+/- 16.4 S.D.) in the placebo group and 56.0% (+/- 23.7) (P = 0.32, NS) in the antioxidant supplemented group. Similarly, there was no difference in the rate of fall between serum aspartate transaminase (AST) concentration in the two groups: the placebo group falling by a mean of 68.9% (+/- 35.2) and the antioxidant supplemented group falling by 70.1% (+/- 10.0) (P = 0.41, NS) over the first 7 days of hospitalization. Alcoholics had low serum concentrations of vitamin E compared with controls (15.6 mg/l +/- 6.2 S.D.) which rose more in the supplemented group over the period of a week (7.7 mg/l +/- 4.4 to 21.6 mg/l +/- 5.1) (a mean rise of 180.5%) compared with the placebo group (8.6 mg/l +/- 6.8 to 9.6 mg/l +/- 5.7)--a mean rise of 11.6% (P = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of antioxidant supplementation on a serum marker of free radical activity and abnormal serum biochemistry in alcoholic patients admitted for detoxification. 830 Oct 30

We have evaluated whether vitamin B6 and C metabolism may be altered by infection in the elderly. Vitamin B6 and C biochemical status has been assessed for times over a period of 21 days (days 0, 7, 14, and 21) in 18 subjects > or = 75 years. The subjects were divided into 3 groups: group I (8 subjects with acute infection), group II (4 malnourished subjects), and group III (6 control subjects). Vitamin B6 status was determined by plasma pyridoxal-5'-phosphate (PLP) and erythrocyte aspartate aminotransferase activation coefficient (alpha-EAST), and vitamin C status by plasma ascorbic acid. During the 3 weeks, vitamins B6 and C values were significantly different between groups: at days 7 and 14, PLP values were significantly higher in group III than in both groups I and II, and alpha-EAST values were significantly higher in group I than in both groups II and III. Plasma ascorbate values were significantly lower in group I than in both groups II and III. These data suggest that an acute catabolic state like infection may influence vitamin B6 and C metabolism. Nevertheless, more work is needed to assert that vitamin B6 and C supplementation may be useful during infection.
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PMID:Vitamin B6 and vitamin C status in elderly patients with infections during hospitalization. 949 Nov 89

Urinary enzyme levels were investigated in rats administered different promoters in their diet for 32 weeks after being initiated by treatment with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine in their drinking water for 4 weeks. All groups were composed of 10 rats each. Group 1: females treated with 3% uracil (100% carcinoma incidence). Group 2: control females kept on basal diet only (0% carcinoma incidence). Group 3: males treated with 5% sodium L-ascorbate (100% carcinoma incidence). Group 4: control males (0% carcinoma incidence). Urine was collected at the end of weeks 12, 24 and 36 and tested for lactate dehydrogenase (LDH), alkaline phosphatase, N-acetyl-beta-D-glucosaminase and aspartate aminotransferase activity. To facilitate comparison, data were related to the corresponding excreted creatinine levels. All measurements were made using a centrifugal automatic analyzer. The urine of rats with cancer lesions (groups 1 and 3) showed significant elevation in all enzyme activities at weeks 24 and/or 36 except for LDH in females (group 1). The M/H ratio of the LDH isozymes was reversed (1.10 +/- 0.10) in the tested rats with carcinomas at week 36. This study thus provides evidence of a correlation between high urinary enzyme levels and cancer development in the rat bladder. Measurement of the tested enzymes might thus provide a method to detect malignant changes in bladder epithelium by direct urine analysis.
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PMID:Elevation of urinary enzyme levels in rat bladder carcinogenesis. 1038 97

The effects of thymoquinone (TQ) and desferrioxamine (DFO) against carbon tetrachloride (CCl4)-induced hepatotoxicity were investigated. A single dose of CCl4 (20 microl/kg, i.p.) induced hepatotoxicity, manifested biochemically by significant elevation of activities of serum enzymes, such as alanine transaminase (ALT, EC: 2.6.1.2) , aspartate transaminase (AST, EC: 2.6.1.1) and lactate dehydrogenase (LDH, EC: 1.1.1.27). Hepatotoxicity was further evidenced by significant decrease of total sulfhydryl (-SH) content, and catalase (EC: 1.11.1.6) activity in hepatic tissues and significant increase in hepatic lipid peroxidation measured as malondialdhyde (MDA). Pretreatment of mice with DFO (200 mg/kg i.p.) 1 h before CCl4 injection or administration of TQ (16 mg/kg/day, p.o.) in drinking water, starting 5 days before CCl4 injection and continuing during the experimental period, ameliorated the hepatotoxicity induced by CCl4, as evidenced by a significant reduction in the elevated levels of serum enzymes as well as a significant decrease in the hepatic MDA content and a significant increase in the total sulfhydryl content 24 h after CCl4 administration. In a separate in vitro assay, TQ and DFO inhibited the non-enzymatic lipid peroxidation of normal mice liver homogenate induced by Fe3+/ascorbate in a dose-dependent manner. These results indicate that TQ and DFO are efficient cytoprotective agents against CCl4-induced hepotoxicity, possibly through inhibition of the production of oxygen free radicals that cause lipid peroxidation.
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PMID:Protective effects of thymoquinone and desferrioxamine against hepatotoxicity of carbon tetrachloride in mice. 1088 36

Activities of hepatic xanthine oxidase (XO) and xanthine dehydrogenase (XD), serum liver enzymes, and reduced glutathione (GSH) were determined in livers of chronic cholestatic rats. The common bile duct was ligated (CBDL) and rats were randomized to either an untreated group or to treatment with allopurinol, a competitive XO inhibitor, or received a tungsten-supplemented diet to inactivate XO and XD, or received antioxidants vitamin C and vitamin E. One group underwent only sham laparotomy. After 4 weeks, in untreated CBDL animals serum aspartate aminotransferase and bilirubin concentrations were significantly elevated and hepatic GSH was significantly decreased when compared with the sham-operated group. Histochemical and enzymatic determinations of XD and XO showed a significant increase in hepatic XO activity after CBDL. Treatment with allopurinol and a tungsten-supplemented, molybdenum-free diet significantly attenuated serum liver enzymes, hepatic XO activity, and improved hepatic GSH levels, whereas vitamins C and E had a positive effect only on hepatic GSH levels. Our results support the hypothesis that cholestasis-induced hepatocellular injury is partially triggered by oxidative processes derived from increased hepatic XO activity. Inhibition and inactivation of XO exerts a hepatocellular protective effect in chronic cholestasis.
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PMID:The impact of hepatic xanthine oxidase and xanthine dehydrogenase activities on liver function in chronic cholestasis. 1089 33

Exposure of human plasma in vitro to gas-phase cigarette smoke (CS) causes a marked modification of plasma proteins as measured by protein carbonyl assay. Aldehydes present in CS may cause this elevation of protein carbonyls by reacting with sulfhydryl groups of proteins. Saliva is the first body fluid to confront the inhaled CS. Thus, in vitro exposure of saliva to nine "puffs" of CS also showed a distinct increase in protein carbonyls. Ascorbate and desferrioxamine mesylate had little effect on protein carbonyl formation, while GSH and N-acetylcysteine considerably inhibited the accumulation of protein carbonyls due to CS exposure. Following the exposure to CS, the activities of several salivary enzymes-amylase, lactic dehydrogenase (LDH), and acid phosphatase-were found to be significantly reduced (34, 57, and 77%, respectively). However, CS had no effect on the activities of aspartate aminotransferase and alkaline phosphatase. Addition of 1 mM of GSH and N-acetylcysteine considerably protected LDH and amylase activities, suggesting that sulfhydryl groups are affected in LDH and amylase. On the other hand, addition of 1 mM ascorbate caused a further loss of LDH and amylase activities, which could be partially prevented by the addition of desferrioxamine mesylate, implicating metal-catalyzed oxidation processes. Finally, loss of acid phosphatase activity was completely unaffected by any of the above antioxidants. It is concluded that the loss of salivary enzyme activities may be due to various agents in the CS that affect the enzyme activities via different mechanisms.
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PMID:Effect of cigarette smoke on salivary proteins and enzyme activities. 1089 39

The purpose of this study was to determine the effects of stage and the number of lactation on plasma ascorbate concentration and to establish the association between plasma ascorbate concentrations and plasma glucose, insulin, nonesterified fatty acids (NEFA), beta-hydroxybutyrate (BHBA), aspartate aminotransferase (AST), milk somatic cell count (SCC), milk yield, and body condition score (BCS) in dairy cows. Holstein cows (n = 193) from three different herds were used in this study. Animals were randomly selected, and assigned to five groups according to stage of lactation (group 1, dry cows; group 2, 1 to 28 d; group 3, 29 to 56 d; group 4, 57 to 140 d; group 5, 141 to 280 d), and the number of lactation (primiparous or multiparous). Plasma ascorbate concentration, plasma glucose concentration, serum insulin concentration, plasma NEFA concentration, plasma BHBA concentration, serum AST concentration, milk SCC, milk yield, and BCS were measured. The results of this study demonstrate that plasma ascorbate concentrations do not change in response to stage of lactation, or number of lactations. Among the several variables studied, none was found that, singly or in combinations, could explain variations in ascorbic acid concentrations.
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PMID:Plasma ascorbate concentrations are not correlated with milk somatic cell count and metabolic profile in lactating and dry cows. 1121 25


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