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)

The effects of simultaneous administration of thiamine, niacin or vitamin B12 with vitamin E on plasma vitamin E levels were studied in 20 adult male volunteers belonging to the low socio-economic class. The effect of vitamin E on the nutritional status of pyridoxine, riboflavin and thiamine as judged by the erythrocyte enzymes, aspartate aminotransferase, glutathione reductase and transketolase, respectively was also studied. None of the members of the B-complex vitamins studied here had any effect on plasma vitamin E levels. This was in contrast to the observation made earlier that pyridoxine and riboflavin can reduce plasma vitamin E. There was a transient reduction in both the basal and stimulated activities of erythrocyte aspartate aminotransferase, the significance of which needs further investigation.
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PMID:Studies on interactions of vitamin E with thiamine, niacin and vitamin B12. 731 77

Cisplatin, a nephrotoxic chemotherapeutic agent, was injected into Sprague Dawley rats, alone or together with cysteine, vitamin E and clonidine. The effects on erythrocyte fragility, serum composition, and kidney and liver enzymes were studied. Cisplatin was administered as two i.p. injections (6 mg/kg body weight) at an interval of 120 hours. The animals were sacrificed 24 hours after the second injection. Erythrocytes were prepared from blood collection with anticoagulant. Serum was prepared from clotted blood, collected without anticoagulant. Kidneys and liver were removed and homogenized, and a supernatant prepared by high speed centrifugation. In cisplatin-treated rats, the serum activities of aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase and alkaline phosphatase were significantly decreased, whereas the activities of isocitric dehydrogenase and glutathione reductase were increased. Also, concentrations of blood urea nitrogen, creatinine, total lipids and magnesium increased while albumin and glucose decreased. Mean osmotic fragility of erythrocytes from cisplatin-treated rats was decreased, while the haematocrit was increased. In the liver, the only change seen was an increased activity of isocitric dehydrogenase. Much greater changes were found in the kidneys, with increased activity of glucose-6-phosphate dehydrogenase and decreased activities of aspartate and alanine aminotransferases, alkaline phosphatase, malic dehydrogenase, sorbitol dehydrogenase and gamma-glutamyltransferase, as well as a decreased phosphorylation to oxidation ratio in the mitochondria, indicating reduced adenosine triphosphate production. Administration of cysteine and vitamin E together with cisplatin partially reversed the uraemia and many of the biochemical changes induced by cisplatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in serum, liver and kidneys of cisplatin-treated rats; effects of antioxidants. 788 81

Subclinical nutritional myopathy was induced in 5-month-old sheep by feeding them a diet low in vitamin E and selenium. Subsequently clinical myopathy was induced by dosing with protected polyunsaturated fatty acids. Plasma activities of creatine kinase (CK), pyruvate kinase, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase and aldolase, enzymes of muscle origin, all remained above their reference ranges in clinically affected sheep, but fluctuated widely. Similar fluctuations occurred in subclinically affected animals, resulting in some activities being within the reference ranges and some above, at different times. Plasma malondialdehyde, an indicator of lipid peroxidation, proved of no diagnostic value. Terminal plasma CK activities were significantly correlated with microscopic damage in the vastus lateralis (VL), but not the vastus intermedius (VI) or the tensor fascia lata (TFL) muscles. AST was the most highly correlated with damage in VI and VL. In two clinically affected sheep successfully treated with an oral dose of alpha-tocopherol acetate all enzymes decreased steadily to within their reference ranges, at rates probably related to their plasma half-lives. These results suggest that measurement of plasma CK activity would be useful in monitoring recovery of treated sheep.
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PMID:Plasma indicators of muscle damage in a model of nutritional myopathy in weaner sheep. 817 46

Experimentally induced salinomycin toxicosis in weanling pigs showed typical clinical signs of an intoxication with a polyether antibiotic. Severe ataxia and recumbency were the most prominent symptoms, which could be attributed to acute skeletal muscle necrosis by estimation of muscle enzyme activities (creatine kinase, aspartate aminotransferase) and histopathological examination. Intoxication had neither influence on concentrations of vitamin E and selenium-dependent glutathione peroxidase in plasma and different organs nor on contents of fatty acids in skeletal muscles. No signs of increased lipid peroxidation in muscle tissue could be found. Prophylactic application of vitamin E or selenium one day before administration of salinomycin as well as treatment on the following days produced no protective effects. The treated pigs showed equal clinical and pathomorphological alterations as the untreated animals, although applications caused a significant increase of alpha-tocopherol and glutathione peroxidase concentrations in blood and different organs.
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PMID:[The effect of treatment with vitamin E or selenium on the course of salinomycin poisoning in swine]. 820 64

Primary cultures of adult rat hepatocytes were incubated (6 to 96 hr) with 50 to 150 mmol/L ethanol, 0.5 mmol/L linoleate, 0.5 mmol/L palmitate, 0.5 mmol/L 4-methylpyrazole, 0 to 25 mumol/L vitamin E phosphate or selected combinations of these agents. Agent-dependent changes in liver cell viability (AST release and reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and function (phospholipid peroxidation, hydrolysis, biosynthesis and triacylglycerol biosynthesis) were determined. The influence of ethanol on liver cell function and viability was dose and incubation time dependent. Short periods (24 hr or less) of exposure to 100 mmol/L ethanol increased liver cell triacylglycerol biosynthesis and phospholipid hydrolysis, peroxidation and biosynthesis without altering cell viability. However, longer periods (72 hr or more) of exposure to 100 or 150 mmol/L ethanol resulted in significant reductions (30% to 50%) in cell viability, function and phosphatidylcholine biosynthesis and content. The ethanol-dependent decreases in cell function and viability were potentiated by linoleate and reduced by vitamin E phosphate, palmitate and 4-methylpyrazole. These results suggest that ethanol-induced liver cell injury in vitro is not a result of ethanol per se, but factors such as acetaldehyde or oxyradicals produced as a consequence of ethanol metabolism. Therefore the incubation of cultured hepatocytes with ethanol may be an appropriate model in vitro for determining the mechanisms by which ethanol intake disrupts liver cell function in vivo.
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PMID:An in vitro model of ethanol-dependent liver cell injury. 827 54

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

Cyclophosphamide, and antineoplastic drug, and vitamin E, the common antioxidant present in the diet, were administered in separate dosages and in combination to animals (rats) with fibrosarcoma, metastatic tumor of the connective tissues, induced. The anticancer drug (20 mg/kg body weight) and the vitamin-E (400 mg/kg body weight) was administered for a period of 28 days from the day of tumor transplantation. The individual and the combined effects of these two substances were investigated by checking the growth of the tumor. Tumor markers like lactate dehydrogenase (LDH), serum glutamate pyruvate transminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT), acid phosphatase, and alkaline phosphatase were analyzed for the changes in their concentration in serum, liver, and kidney to assess the success of the therapy. The increased level of the enzymes in the fibrosarcoma-suffering rats (GPII) was reduced by cyclophosphamide treatment (GP III) and vitamin E administration (GP IV). Among the treated groups, the combination therapy (GP V) showed greater efficacy in the treatment of fibrosarcoma than did individual administration, as there was more reduction in the levels of enzymes in Group V than those in to Groups III and IV. The enzyme levels were brought to near the normal level.
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PMID:Effect of administering cyclophosphamide and vitamin E on the levels of tumor-marker enzymes in rats with experimentally induced fibrosarcoma. 853 10

In a randomized, double-blind, placebo-controlled trial, the effects of combined treatment with the antioxidant vitamins A (50,000 IU/day), vitamin C (1,000 mg/day), vitamin E (400 mg/day), and beta-carotene (25 mg/day) were compared for 28 days in 63 (intervention group) and 62 (placebo group) patients with suspected acute myocardial infarction. After treatment with antioxidants, the mean infarct size (creatine kinase and creatine kinase-MB gram equivalents) was significantly less in the antioxidant group than in the placebo group. Serum glutamic-oxaloacetic transaminase decreased by 45.6 IU/dl in the antioxidant group versus 25.8 IU/dl in the placebo group (p < 0.02). Cardiac enzyme lactate dehydrogenase increased slightly (88.6 IU/dl) in the antioxidant group compared with that in the placebo group (166.5 IU/dl) (p < 0.01). QRS score in the electrocardiogram was significantly less in the antioxidant than in the placebo group. The following levels increased in the antioxidant group versus the placebo group, respectively: plasma levels of vitamin E increased by 8.8 and 2.2 mumol/L (p < 0.01), vitamin C increased by 12.6 and 4.2 mumol/L (p < 0.01), beta-carotene increased by 0.28 and 0.06 mumol/L (p < 0.01), and vitamin A increased by 0.36 and 0.12 mumol/L (p < 0.01). Serum lipid peroxides decreased by 1.22 pmol/ml in antioxidant versus 0.22 pmol/ml in the placebo group (p < 0.01). Angina pectoris, total arrhythmias, and poor left ventricular function occurred less often in the antioxidant group. Cardiac end points were significantly less in the antioxidant group (20.6% vs 30.6%, respectively). These results suggest that combined treatment with antioxidant vitamins A, E, C, and beta-carotene in patients with recent acute myocardial infarction may be protective against cardiac necrosis and oxidative stress, and could be beneficial in preventing complications and cardiac event rate in such patients.
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PMID:Usefulness of antioxidant vitamins in suspected acute myocardial infarction (the Indian experiment of infarct survival-3) 931 5

A total of 300 female broiler chickens were reared from day-old to 10 d of age on the same starter diet. Then they were divided into five groups, receiving a control diet (Group 1) relatively rich in fat (14.3%) and unsaturated fatty acids (87.6%) and standardized with respect to vitamins and minerals, supplemented with 100 mg (Group 2) and 500 mg (Group 4) of RRR-alpha-,gamma-,delta-tocopheryl acetate/kg feed (40.6% alpha-, 41.1% gamma-, 18.3% delta-) or 100 mg (Group 3) and 500 mg (Group 5) all-rac-alpha-tocopheryl acetate/kg feed until slaughter at 6 wk of age. No differences between the supplemented groups were observed with respect to weight gain, feed consumption, packed cell volume (PCV), plasma enzyme activities of creatine kinase (CK) and glutathione peroxidase (GSH-Px), fatty acid composition, and enzyme activities of citrate synthase (CS), and total lactate dehydrogenase (LDH), and 3-OH-acyl-coenzyme A-dehydrogenase (HAD) of breast (Pectoralis major) and thigh (Gastrocnemius interna) muscle. Increasing levels of alpha-, gamma-, and delta-tocopherol were found in blood plasma with increasing dietary levels of these tocopherols. Only alpha-tocopherol was detectable in skeletal muscle and in higher concentrations in thigh than in breast muscle. Hemolysis in vitro and plasma activity of aspartate aminotransferase (ASAT) were lower (P < .01) in Groups 2 and 4 than in Groups 3 and 5. Interactions were observed between dietary type and concentration of tocopherols for plasma CK, GSH-Px, Na+, and K+. No measurable excretion of ethane and pentane was observed in any of the groups. The findings indicate that the oxidative stress in the live animals was minimal. The mixture of natural source RRR-alpha-,gamma-,delta-tocopherols was as efficient in protecting the live chickens as the all-rac-alpha-tocopheryl acetate, when provided on a weight basis as judged from the chosen in vivo parameters of vitamin E status.
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PMID:Supplementation of broiler diets with all-rac-alpha- or a mixture of natural source RRR-alpha-,gamma-,delta-tocopheryl acetate. 1. effect on vitamin E status of broilers in vivo and at slaughter. 882 89

Because of the very low concentrations of selenium in the dry matter of grass, grass silage, hay and maize silage Slovenian dairy herds need to be supplemented with selenium. Selenium in the form of mineral and feed mixtures maintained adequate mean (sd) blood serum selenium concentrations of 43.9 (27.6) to 65.3 (18.5) micrograms/litre in lactating cows, but in late lactation and in the dry period when only mineral mixtures were used, about 60 per cent of the cows had marginal serum selenium concentrations, mainly because of the low intake of the mineral supplement. In 18 herds which were either unsupplemented or irregularly supplemented with selenium, the mean (sd) concentrations in blood serum were 13.7 (5.5) micrograms/litre and 17.4 (9.2) micrograms/litre, respectively, for selenium and 2.98 (2.72) mg/litre and 1.62 (1.73) mg/litre for vitamin E, indicating that under extensive farming conditions in Slovenia the lack of both micronutrients may be responsible for nutritional muscular dystrophy in calves. Among 37 clinical cases, cardiorespiratory signs predominated in 25 of the calves and skeletal myopathy was dominant in 12. A very low mean serum selenium concentration [9.7 (7.2) micrograms/litre] and typically high activities of aspartate aminotransferase (AST) [1125 (373) U/litre] and creatine kinase (CK) [9169 (3681) U/litre) were observed for the myocardial form of the disease, and 2797 (550) U/litre and 22,650 (13,500) U/litre were observed for the skeletal form of the disease. A highly significant (P < 0.0001) difference in the selenium concentration of liver dry matter between the regularly supplemented [402 (207) micrograms/kg] and irregularly supplemented [173 (69) micrograms/kg] herds was observed. If a minimum value of 300 micrograms/kg of liver dry matter is accepted as the criterion for the determination of adequate selenium status, 93 per cent of the samples from the irregularly supplemented herds were selenium deficient. A similar proportion was estimated to be selenium deficient when the criterion was taken to be 30 micrograms selenium/litre of blood serum.
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PMID:Assessment of selenium and vitamin E deficiencies in dairy herds and clinical disease in calves. 891 12


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