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 aim of this study was tracing of changes in the activity of glutathione peroxidase (GSHPx), glutathione transferase (GSH S-Tr), aspartate aminotransferase (AspAT) and alanine aminotransferase (A1AT) in the brain as a result of diet enrichment with antioxidants: selenium (Se), vitamin E and vitamin B15 (pangamic acid). The experiment was carried out on Wistar rats with initial body weight 150 g. Following prolonged enrichment of diet with Se (0.1 ppm of sodium selenite), vitamin E (6 mg/100 g of diet) and vitamin B15 (2.5 mg/100 g of diet) the following results were obtained. The activity of GSHPx in brain microsomes was not changed after one year of vitamin E administration when it was measured against hydrogen hydroxide and against cumene hydrochloride; vitamin E administration increased the activity of GSH S-Tr in the cytoplasmic fraction of brain cells. Diet enrichment with selenium increased after 12 and 18 months the activity of GSHPx measured against both substrates, and GSH S-Tr activity increased considerably. Presence of vitamin B15 in diet reduced GSHPx activity after one-year or longer administration, after 18 months the activity of GSH S-Tr was reduced also. No changes were noted in the activity of AspAT and A1AT.
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PMID:The effect of long-term enrichment of diet with selenium, vitamin E and B15 on the activity of certain enzymes in rat brain. 345 69

Feeding a basal diet free of vitamins E and C to weanling male rats for 8 months resulted in biochemical changes characteristic of vitamin E deficiency. These included increased liver thiobarbituric acid values; decreased blood GSH levels, plasma vitamin E levels, and glutathione peroxidase activities; and increased activities of plasma pyruvate kinase, glutamic-oxaloacetic transaminase, creatine kinase, lactic dehydrogenase, and malic dehydrogenase. Tube-feeding vitamin C for 21 days resulted in partial reversal effects on the above parameters except activities of glutathione peroxidase, lactic dehydrogenase, and malic dehydrogenase. The results suggest that vitamin C may spare in part the metabolism of vitamin E through its antioxidant property.
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PMID:Vitamin C partially reversed some biochemical changes produced by vitamin E deficiency. 382 80

Selenium deficiency has been implicated as a cause of hepatic injury, possibly from accentuated lipoperoxidation due to decreased activity of the selenoenzyme, glutathione peroxidase. Because of possible clinical and biochemical links between selenium and alcohol, we performed nutritional assessment and assayed red blood cell, plasma, and whole blood selenium by spectrofluorometry in 27 normals (group I), 30 asymptomatic alcoholics on admission to a detoxification unit, (group II) and 16 alcoholics with severe liver disease (group III). We found a mean (+/- SD) whole blood selenium of 0.109 micrograms/ml +/- 0.014 for group I vs 0.076 +/- 0.010 for group II (P less than 0.001), and 0.047 +/- 0.006 for group III (P less than 0.001 vs group I and II). For plasma, the mean (+/- SD) selenium was 0.095 micrograms/ml +/- 0.016 for group I versus 0.065 micrograms/ml +/- 0.012 in group II and 0.038 micrograms/ml +/- 0.007 in group III (All P less than 0.001). Calculated red blood selenium levels were also significantly reduced in alcoholics versus controls. Whole blood and plasma selenium correlated directly with serum albumin. For whole blood selenium versus albumin, r = 0.73 (P less than 0.01), and for plasma selenium versus albumin, r = 0.71 (P less than 0.01). A significant inverse correlation was noted between whole blood selenium and the height of the total serum bilirubin (r = -0.46), alkaline phosphatase (r = -0.50), and AST (r = -0.51) (P less than 0.01 for all). Among alcoholics admitted for detoxification, selenium was diminished despite the absence of severe malnutrition, as determined by standard nutrition assessment parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low blood selenium levels in alcoholics with and without advanced liver disease. Correlations with clinical and nutritional status. 402 13

A total of 96 crossbred pigs received various levels of sodium selenite to determine the effect of dietary selenium (Se) on growing swine fed corn-soybean meal diets. Levels of supplemental Se were 0, 4, 8, 12, 16 and 20 micrograms/g. There were linear decreases (P less than .01) in both gain and feed intake with increasing levels of dietary Se. Feed/gain increased numerically as dietary Se increased. Hair Se increased quadratically (P less than .01) and blood Se increased linearly (P less than .01) with increasing level of dietary Se. Cell volume and hemoglobin were not affected by dietary treatment. Increasing dietary Se significantly increased glutathione peroxidase (GSH-Px), glutamic-oxalacetic transaminase (GOT). and glutamic-pyruvic transaminase (GPT). External signs of selenosis were noted in some pigs fed 12 or 20 micrograms/g of Se. The toxic level of Se in a corn-soybean meal diet for crossbred pigs appears to be between 4 and 8 micrograms/g. Of variables studied, growth rate was the most sensitive indicator of chronic selenosis in swine.
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PMID:Toxic effects of selenium on growing swine fed corn-soybean meal diets. 654 46

The activity of glutathione peroxidase (GSH-Px) was measured in the erythrocytes of 600 Thoroughbred horses in training; the selenium concentrations in whole blood and serum was measured in over 80 of these Thoroughbreds. A quadratic relationship was demonstrated between erythrocyte GSH-Px and whole blood or serum selenium concentration. There was no significant difference in the activity of aspartate aminotransferase, creatine kinase, or gamma-glutamyl transferase in the serum of Thoroughbreds with high erythrocyte GSH-Px activity (more than 25 u/ml) when compared with those with low erythrocyte GSH-Px activity (less than 15 u/ml).
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PMID:Selenium status of thoroughbreds in the United Kingdom. 708 98

Day-old poults from hens depleted of Se were fed low-Se basal diets (containing corn, soybean meal, and torula yeast but no added vitamin E) with graded levels of Se supplied by Na2SeO3 or seleno-DL-methionine for 28 and 35 days in Experiments 1 and 2, respectively. Adding .04 ppm Se to the basal diet significantly increased body weight and reduced both the incidence of gizzard myopathy and plasma glutamic-oxaloacetic transaminase (PGOT) activity. Further plasma Se and Se-dependent glutathione peroxidase (SeGSHpx) were elevated by increasing levels of dietary Se. There were no differences in these parameters due to the Se compound fed. Plasma SeGSHpx was significantly correlated with both dietary and plasma Se levels. Poults fed selenomethionine had significantly higher concentrations of Se in the gizzard, breast muscle, and pancreas, but not in the liver and heart, compared to poults fed Na2SeO3. These studies indicate that the utilization of Se in both Na2SeO3 and selenomethionine is approximately equal in young turkey poults.
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PMID:Comparative effects of sodium selenite and selenomethionine upon nutritional muscular dystrophy, selenium-dependent glutathione peroxidase, and tissue selenium concentrations of turkey poults. 708

1. Glutatione peroxidase activity (EC 1.11.1.9) and erythrocyte stability were measured in Friesian bull calves which were given for 36 weeks semi-purified diets either adequate or low in selenium or vitamin E or both. 2. Dietary Se or vitamin E content had no effect on growth rate and haematlogical values. None of the calves exhibited clinical deficiency symptoms and serum aspartate amino transferase (EC 2.6.1.1) and creatine phosphokinase (EC 2.7.3.2) activities remained normal. Heart and skeletal muscles of all calves appeared macroscopically and microscopically normal ato autopsy. 3. Glutathione peroxidase activity in plasma, blood and other tissues, except the testis, was significantly lower in calves receiving low dietary Se but was independent of dietary vitamin E content. 4. Plasma vitamin E levels decreased rapidly and to very low levels in calves given low vitamin E diets irrespective of the Se content of the diet. 5. A low dietary vitamin E intake increased the susceptibility of erythrocytes to auto- and peroxidative haemolysis whereas a low Se intake in the presence of adequate vitamin E did not. However, erythrocytes from calves receiving low Se and low vitamin E were more susceptible to peroxidative haemolysis than erythrocytes from calves receiving low vitamin E and adequate Se. The effect of dietary vitamin E content on osmotic haemolysis induced by hypotonic saline was variable. 6. The results suggest that measurement of blood glutathione peroxidase activity and the susceptibility of erythrocytes to auto- or peroxidative haemolysis could be used for the differential diagnosis of subclinical Se and vitamin E deficiency in ruminants.
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PMID:Glutathione peroxidase activity and erythrocyte stability in calves differing in selenium and vitamin E status. 728

Acute and chronic effects of Se as sodium selenite given as a supplement in the drinking water of Sprague-Dawley rats for 35 d, 1 yr, and 2 yr are compared. For the 35-d study the experimental groups were untreated controls and rats supplemented with 1, 4, 8, 16, and 64 ppm Se. Survival was 100% in the control and 1 and 4 ppm groups, decreased in the 8 and 16 ppm groups, and was zero in the 64 ppm group. Body weights increased and were equivalent in the control and 1 and 4 ppm groups and substantially decreased in the 16 and 64 ppm groups., Serum alkaline phosphatase and glutamic-oxaloacetic transaminase (SGOT) increased with 16 ppm Se and higher supplements. Se toxicity was apparent in microscopic pathology showing liver congestion, fatty degeneration of parenchymal cells, and necrosis. In the chronic studies untreated controls are compared with rate receiving 4 ppm Se in the drinking water. In general, the weight gains throughout were equivalent for both groups. The 1-yr survival in each was above 90% and the 2-yr survival above 50%. With increased age there was a slight reduction in hemoglobin and white blood cells. The latter effect was greater in Se-treated then in control rats. Several serum components were equivalent in both groups, including alkaline and acid phosphatase, SGOT, protein, glucose, and sialic acid. Liver glutathione peroxidase was half and Se levels in the Se-treated rats were twice those in the controls. Data are presented for male rats in the chronic study with occasional reference to data on females. The parameters measured in the chronic study are highly dependent on the age of the rat when Se-supplemented drinking water is initiated.
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PMID:Toxicological effects of sodium selenite in Sprague-Dawley rats. 733 30

Se as sodium selenite was administered by gavage (three consecutive times) and as drinking water supplements for 46 d to male and female Swiss mice. With respect to survival in 7-wk-old mice, Se was less toxic in males than in females when gavaged. Drinking water supplements of 1-64 ppm Se resulted in 1 male and 1 female death in mice first given Se at 7 wk of age. Se supplements to the drinking water of adult (18-wk-old) mice was less toxic in females. All young (7-wk-old) and adult (18-wk-old) mice provided 1-16 ppm Se in the drinking water survived the 46-d treatment, but in adult mice 64 ppm Se significantly reduced survival. Only 64 ppm Se supplements caused a sharp reduction in body weight in young and adult mice of both sexes. Supplements of 1-8 ppm Se in all mice elicited growth responses similar to those of untreated controls. Occasional liver and kidney congestion, liver necrosis, parenchymal cell degeneration, and bile duct proliferation were observed in control and treatment groups. Serum alkaline phosphatase and glutamic-oxaloacetic transaminase (SGOT) increased with 32 ppm Se and higher supplements. Survival, growth, serum enzymes, and pathology were normal in untreated controls and in mice of growth ages and sexes give 1, 4, and 8 ppm Se supplements. A chronic toxicity study was conducted in female Swiss mice given 1, 4, and 8 ppm Se supplements for 50 wk. The survival of Se-treated groups was more than 90% and that of controls was only 72% after 50 wk. All mice gained weight, but the group treated with 8 ppm Se gained half as much as other groups. Both liver Se and glutathione peroxidase activity increased in Se-treated mice compared to controls at 25 and 50 wk. A reduced white blood cell count and increased alkaline phosphatase and SGOT suggested a mild toxic effect of the 8 ppm Se supplement in the chronic study.
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PMID:Toxicological effects of sodium selenite in Swiss mice. 733 31

It has recently been proposed that a depletion of glutathione (GSH) may be a contributing factor to viral persistence and resistance to interferon-alpha (IFN-alpha) therapy in chronic hepatitis C virus (HC) infection. The aim of this study was: (1) to compare plasma GSH levels in patients with chronic HCV infection and normal healthy controls; and (2) to correlate GSH levels with liver histology and serum HCV RNA levels. Twenty-four patients with compensated chronic hepatitis C and 27 healthy subjects were studied. Serum and heparinized plasma were prospectively prepared and frozen within 1 h of collection. Plasma glutathione and glutathione peroxidase (GP) levels were measured spectrophotometrically. The serum HCV RNA level was quantitated by the branched chain DNA signal-amplification assay. Plasma GSH levels were not decreased in patients with chronic HCV infection but were actually greater than in controls (control 1.27 +/- 0.12 micrograms ml-1, HCV 1.62 +/- 0.11 micrograms ml-1, P < 0.05). There was also no difference in plasma GP activity between these two groups (control 0.233 +/- 0.007 U ml-1, HCV 0.230 +/- 0.007 U ml-1). Among the patients with chronic HCV infection, there was no correlation between either plasma GSH or GP levels and the serum alanine aminotransferase (ALT) or aspartate aminotransferase (AST), serum HCV RNA level, or liver histology. This study demonstrates that chronic HCV infection does not decrease the plasma GSH and GP levels.
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PMID:Plasma glutathione concentration in patients with chronic hepatitis C virus infection. 748 49


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