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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.
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PMID:Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence. 359 58

Partial ileal bypass (PIB) surgery is a method for the treatment of familial hypercholesterolaemia in man. Since the rabbit is frequently used as an animal model in experimental studies on PIB, we have investigated the long-term effects of this surgical procedure on the health status of rabbits. Forty-eight weeks after surgery plasma and liver cholesterol levels were decreased by about 40%. The inner diameter of the bypassed ileum was drastically reduced, unlike its length. The bypassed segment did not show clear histological abnormalities. The microflora of the caecum was similar in control and PIB rabbits. PIB did not influence liver histology. The bile of the rabbits with PIB was less lithogenic than that of control animals. Blood haemoglobin levels, haematocrit values and plasma concentrations of alkaline phosphatase, alanine aminotransferase, gamma-glutamyl transferase and lactate dehydrogenase were not changed after PIB. Plasma levels of albumin, creatinine, calcium, phosphorus, vitamin B12 and folic acid were not significantly affected by PIB. Rabbits with PIB had significantly higher plasma levels of bilirubin and zinc than control rabbits, but plasma vitamin E concentrations were significantly lower. These results may be of importance for further studies on the effects of PIB in rabbits.
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PMID:Long-term effects of partial ileal bypass on the health status of rabbits. 370 23

After 7 weeks on a vitamin E deficient diet plasma and liver content of vitamin E were reduced by 60-70%. This treatment, a two week chronic ethanol intake or their combination all caused a significantly higher level of liver glutathione as compared to untreated rats. The chronic ethanol treatment also increased the activity of both alcohol dehydrogenase and aldehyde dehydrogenase and this effect was potentiated by vitamin E deficiency. The activity of the mitochondrial enzyme glutamate dehydrogenase was reduced both by vitamin E deficiency and by ethanol treatment. The activity of the cytosolic alanine aminotransferase was, on the other hand, markedly elevated by vitamin E deficiency, but this effect was completely abolished by ethanol treatment. Several similarities between the effects of chronic ethanol intake and vitamin E deficiency indicates that a poor vitamin E status may potentiate some of the ethanol-induced derangements in the liver.
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PMID:Combined vitamin E deficiency and ethanol pretreatment: liver glutathione and enzyme changes. 378 47

A male born to first cousins presented at 12 months with hypocalcemic convulsions, rickets, epistaxis due to vitamin K deficiency, and extremely low serum levels of beta-carotene and vitamin A. Liver function was altered moderately (glutamic-oxaloacetic transaminase, 55 U/L; glutamic-pyruvic transaminase, 37 U/L; lactate dehydrogenase, 255 U/L; alkaline phosphatase, 437 U/L). To correct the deficiencies, 8,000 IU vitamin D/day, 10,000 IU vitamin A/day, and intramuscular administration of vitamin K1 were required. At 9 years, he presented signs of neuromuscular affection, and the serum vitamin E level (measured for the first time) was extremely low. Classic lipid malabsorption syndromes (abetalipoproteinemia, chronic cholestasis, mucoviscidosis, coeliac disease, Whipple's disease) were excluded by appropriate examinations. Composition of duodenal bile acids was characterized by undetectable levels of cholic acid metabolites, and only chenodeoxycholic acid metabolites were present. Serum total bile acid concentration was normal, with an atypical low cholic acid/chenodeoxycholic acid ratio and abnormal presence of 3 beta-OH-delta 5-cholenic acid and 6-OH-bile acids. Urinary bile acid composition was also characterized by elevated 6-OH-bile acids. Known enzymopathies of the bile acid synthetic pathway were excluded (cerebrotendinous xanthomatosis, cerebro-hepato-renal syndrome of Zellweger, coprostanic acidemia). Bile acid pool sizes were determined by using stable isotopes: cholic acid pool size [2.90 (N, 32 +/- 16) microM/kg] and chenodeoxycholic acid pool size [10.8 (N, 32.6 +/- 9.9) microM/kg] were extremely low; fractional turnover rates of both bile acids were in a normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malabsorption of liposoluble vitamins in a child with bile acid deficiency. 379 31

The biochemical profile [levels of calcium, phosphorus, magnesium, chlorides and iron, the activities of alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and the concentrations of total protein, albumin, cholesterol, urea, glucose, and vitamins A and E] was studied in the blood serum of 40 anoestrous and 40 control inseminated animals in a production herd with an increased occurrence of anoestrus in gilts. The anoestrous gilts showed significantly lower levels of albumin (P less than 0.01) and glucose (P less than 0.01) and ALP activity (P less than 0.05), and significantly higher concentrations of urea (P less than 0.01), vitamin A (P less than 0.01) and vitamin E (P less than 0.05) and ALT activity (P less than 0.05), as compared with the inseminated controls. An extended enzymatological examination consisting of the evaluation of the activities of ALP, AST, ALT and gamma-glutamyl transferase (GMT) was performed in another set of 22 anoestrous and 20 mated gilts. The anoestrous gilts showed a statistically significant increase in the activities of AST (P less than 0.01), GMT (P less than 0.01) and ALT (P less than 0.05) and an insignificant increase in the activity of ALP in comparison with the control animals. The comparison of the obtained values of the studied biochemical criteria with literary data indicated a lower concentration of magnesium and a higher ALP and ALT activities in the anoestrous and inseminated gilts in both groups under study. A high acidity of fat and a medium to high fungus infestation (Mucor sp., Aspergillus sp.) were found by chemical and mycological examination of the administered feed mixtures. The histological examination of the ovaries of anoestrous animals showed cystically degenerative changes, proliferations of fibrous elements, and partial atrophy of ovarial cortex. It has been inferred from the observations that mycotoxins may be involved in the increase in the occurrence of anoestrus, either by a direct effect on sexual organs or by impairing the function of liver which, secondarily contributes to the rise of ovarial dysfunctions.
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PMID:[Changes in selected biochemical indicators in blood serum in anestrous gilts]. 640 28

The seasonal characteristics of the efficacy of vitamin E and sodium selenite in tetracycline affections of the liver were studied on 128 noninbred male albino rats. It was shown that in comparison to vitamin E sodium selenite more actively retarded activation of lipid peroxidation in the liver and activation of alanine aminotransferase and alkaline phosphatase in the blood serum in autumn and winter. A more pronounced inhibition of the increased levels of the dienic conjugates and alanine aminotransferase was observed in spring and summer and malonic dialdehyde and aspartate aminotransferase in summer by tocopherol acetate as compared to sodium selenite. The level of the thiol-disulfide equilibrium on the separate use of the drugs in spring and summer was higher than the control one. However, it did not reach the control level in autumn and winter. The combined use of sodium selenite and vitamin E prevented the toxic effect of tetracycline on the liver in autumn, spring and summer. Still, in the winter no such prevention was observed. The mechanisms of the seasonal differences in the tetracycline effect on the liver and the efficacy of the antioxidants in such affections are discussed.
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PMID:[Seasonal characteristics of the effectiveness of vitamin E and sodium selenate in tetracycline-induced liver damage]. 652 88

Studies on albino rats showed that high doses of tetracycline-induced damages of the liver evident from increased activity of serum enzymes (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) and inhibition of bile secretion, synthesis and secretion of bile acids and cholesterol excretion. Administration of vitamin E, sodium selenite, infusion of Astragalus L. and especially vitamin E combinations with sodium selenite markedly or completely arrested the occurrence of hepatotoxic properties of tetracycline. It is suggested that the use of vitamin E combinations with selenium-containing preparations is advisable in the prophylaxis and treatment of tetracycline-induced damages of the liver.
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PMID:[Vitamin E and selenium-containing preparations in the prevention treatment of tetracycline-induced lesions of the liver]. 663 74

In the present study we first demonstrated that T-2 toxin markedly stimulated lipid peroxidation specifically in the liver of rats. The amount of lipid peroxides in the liver, estimated by the thiobarbituric acid (TBA) method, increased dose dependently, being proportional to the extent of its acute toxicity measured by various parameters in rats fed a commercial diet. Further, to elucidate the mechanism of lipid peroxidation and its role in hepatic injury caused by T-2 toxin, time-course studies on the correlation between lipid peroxide content and some biological and histopathological data were undertaken in rats given 4 mg of the toxin/kg perorally. The TBA reactive substances in the liver began to increase after 6 hr. However, much earlier than this there were some other alterations, which included decreases in the amount of cytochrome P-450 in the liver, of GPT (thereafter an increase) and phospholipids in the plasma, and of basophilic masses in the hepatocytes (arrayed as a rough endoplasmic reticulum in the electron micrograph). The vitamin E-deficient study showed that vitamin E markedly inhibited the stimulative effect of T-2 toxin on lipid peroxidation, but not diminish any other measured parameters of the injury. The toxin-induced stimulation of lipid peroxidation does not appear to be caused by activation of microsomal NADPH-cytochrome c reductase nor by a decrease in the level of cytosolic glutathione peroxidase. These results suggest that T-2 toxin might induce some alteration of the membrane structure and consequently might stimulate lipid peroxidation in situ.
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PMID:Elevation of thiobarbituric acid values in the rat liver intoxicated by T-2 toxin. 672 68

The aim of this study was to evaluate oxygen-dependent hepatic reperfusion injury in humans following orthotopic liver transplantation. To this end, a number of blood indices of impaired tissue redox balance were monitored in 19 adult patients for 3 weeks after liver transplantation. Both red cell malonaldehyde and plasma lipid peroxides increased significantly soon after organ reperfusion. This finding was consistently accompanied by decreased plasma vitamin E and red cell total glutathione. A peak of oxidative stress, as measured by the parameters monitored, was evident within 24 h after reperfusion, together with a maximum expression of cytolysis, as measured by plasma alanine aminotransferase. The occurrence of redox imbalance after hepatic reperfusion was shown to be linearly related to irreversible cell damage. As regards the low plasma levels of the two antioxidants after reperfusion, only that of vitamin E appeared statistically related to oxidative stress. With the background of an increasing body of proof, mainly from animal models, the involvement of toxic oxygen metabolites in hepatic cytolysis following orthotopic liver transplantation appears likely. The statistical correlation among the markers of redox imbalance monitored indicates their combined use in further investigation.
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PMID:Oxidative damage in human liver transplantation. 755 45

Antioxidative activity of ubiquinone-10, exceeding the level of that of vitamin E more than five times and anticytolytic activity of vitamin E and particularly of ubiquinone-10 manifested in decreasing activities of blood serum alanine aminotransferase and histidineammoniumlyase, which might be determined only during toxic liver damage, have been demonstrated. The activity of histidineammoniumlyase was considerably decreased under the effect of vitamin E and particularly in the presence of ubiquinone-10. Decreasing of activity of blood serum enzyme markers of cytolysis of hepatocytes is connected with the hepatocytes biomembrane stabilizing effect of antioxidants which was confirmed by the electron microscope investigation method. The evidence of safety of intact cellular and subcellular membranes and activation of compensative and regenerative processes in hepatocytes was also represented.
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PMID:[The anticytolytic activity of ubiquinone-10 in a liver lesion from chlorinated hydrocarbons]. 775 66


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