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)

The morphological, histochemical and biochemical changes in the liver of rats challenged with a single intraperitoneal injection of the toxin of lupinosis were investigated. The resulting injury is biphasic. The initial non-specific phase lasts for a few days, affects mainly the centrilobular region and is characterised by mitochondrial swelling, lipid accummulation and autophagosome formation. In addition, the hepatic concentrations of OCT, LDH, SDH, and AST fall while that for ALP increase. This is accompanied by a rise in the serum concentration of many of these enzymes. The second phase lasts longer and is characterised by phenomena indicative of abnormalities in hepatocytic division. Normal and abnormal metaphase as well as multinucleated hepatocytes falls. The possibility that the toxin of lupinosis interferes with microtubular units is considered.
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PMID:The pathogenesis of lupinosis in the rat. 125 1

The authors report on occurrence, causes and diagnostics of liver affections observed in fattening bulls in Ukrainia between 1982 and 1988. For this purpose, 2747 bulls in 10 fattening plants had been controlled clinically once during the last month of their final fattening period (lasting, according to the feeding schedule, from the 4th until the 12th, or from the 6th until the 18th month of life), and 1318 of them were controlled for eventual hepatic lesions at slaughter. The authors found an increase in liver affections during the final fattening period. The type of lesion found preferentially in the different fattening plants showed a certain correlation with feeding used in these: The prevalence of liver lesions (i.e. in 87.2% of the animals controlled) were found in fattening bulls fed cereal branstraw-pellets; among these, liver abscesses were most frequent (i.e. 55.2% of all lesions observed in this group). Steatosis of the liver was prevalent in fattening bulls receiving eating offalls (i.e. 82.7% of all lesions found in that group), whereas liver cirrhosis was prevalent in fattening bulls fed with sugar beet chips-silage. In Holstein-bulls, liver lesions were about double as frequent as in Fleckvieh-bulls (i.e. 37.3 and 16.7% of the livers controlled were found involved, respectively). Diagnostical value of several clinical parameters controlled is discussed (i.e. size and sensitivity of liver percussion field, activity of SDH, LDH, AST and ALT in serum, serum concentration of vitamin A, D3-25 and E, concentration of Vitamin A in liver, and concentration of cholic acids and of their glucoconjugates in bile).
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PMID:[Liver diseases of fattening bulls]. 150 64

Extracts of homologous organs (liver, muscle) and of colostrum were infused intravenously in cattle of two different age groups: heifers (n = 9, each preparation was infused in 3 animals) and calves (n = 6, preparations from liver and muscle were infused in 3 animals each). Parameters of elimination kinetics were determined for some clinically relevant enzymes. Enzyme elimination was quicker in the younger animals. The volume of enzyme distribution was comparable to plasma volume. Biological half-lives in calves and heifers respectively were: CK from muscle 3.46 +/- 0.65 h and 8.27 +/- 3.27 h, AST from muscle 9.74 +/- 1.38 h and 33.48 +/- 3.74 h, AST from liver 14.99 +/- 0.81 h and 16.71 +/- 0.58 h, GLDH from liver 14.61 +/- 1.88 h and 25.09 +/- 4.13 h, SDH from liver 13.95 +/- 2.25 h and 17.68 +/- 0.81 h, GGT from colostrum 1.69 +/- 0.95 h (only heifers).
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PMID:[Elimination kinetics of several clinically relevant enzymes in the blood plasma of cattle after intravenous bolus infusion of homologous preparations]. 163 72

It has been shown that BrCCl3 is a more potent hepatotoxin than CCl4. Pretreatment with nontoxic dietary levels of chlordecone (CD) results in amplification of BrCCl3 hepatotoxicity. The objective of this research was to investigate and compare the histopathological alterations during a time course after a low dose of BrCCl3 alone and in combination with dietary CD. Male Sprague-Dawley rats were maintained on 10 ppm dietary CD or normal diet for 15 days. On day 16, they received a single ip dose (30 microliters/kg) of BrCCl3 in corn oil (CO) vehicle or corn oil alone. Blood and liver samples were collected at 0, 3, 6, 12, 24, 36, 48, 72, 96, and 120 hr for serum enzymes and histopathological examination, respectively. Serum enzymes (SDH, ALT, AST) were significantly (p less than 0.05) elevated in rats receiving the CD + BrCCl3 combination in comparison to BrCCl3 alone. For 48 hr, a continuous increase in serum enzyme activities was detected in rats treated with CD + BrCCl3 combination, but not in the rats receiving other treatments (ND + BrCCl3, ND + CO, or CD + CO). The most extensive hepatolobular necrosis was observed in rats treated with the CD + BrCCl3 combination. Thirty-six hr after the administration of BrCCl3 to rats maintained on normal diet, high mitotic activity was observed, which continued through 72 hr resulting in complete restoration of hepatolobular structure. In contrast, rats receiving the combination of CD + BrCCl3 exhibited minimal and belated hepatomitotic activity for a short period of time, resulting in progressive hepatic failure, culminating in animal death. In conclusion, hepatotoxicity of a low dose of BrCCl3 alone appeared to be overcome via stimulated hepatocellular regeneration and hepatolobular restoration. CD appears to amplify BrCCl3 hepatotoxicity via interference with this hormetic mechanism, permitting a progressive and continued hepatic injury leading to complete hepatic failure, culminating in animal death.
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PMID:Bromotrichloromethane hepatotoxicity. The role of stimulated hepatocellular regeneration in recovery: biochemical and histopathological studies in control and chlordecone pretreated male rats. 170 15

Nickel deficiency was induced in 2- to 4-year-old goats by feeding 0.1 mg Ni/kg dry matter with a semisynthetic diet. The control group consumed 5.0 mg Ni/kg d.m. Activity of several enzymes (SDH, LDH, HBDH, AST, ALT, ALD, CK, CHE) was determined in the serum, liver, heart and kidneys. Serum urea-N level was also measured and transmission electron microscopic (TEM) examinations were performed. Signs characteristic of nickel deficiency (retarded growth, increased mortality of dam and offspring, parakeratosis of the skin) appeared in the low-nickel group. The activity of SDH and ALD, as well as the level of urea-N was significantly lower in the serum of Ni-deficient animals than in the control. Ni-deficient animals also had significantly lower enzyme activities in the heart (SDH, HBDH, AST, ALT, ALD and CK), liver (SDH and CHE) and kidneys (HBDH and CK). Electron micrographs showed degeneration of cardiac and skeletal muscle in the Ni-deficient animals. Ni deficiency elicited changes primarily in the heart and these resulted in depressed activity of several enzymes.
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PMID:Effect of nickel deficiency on biochemical variables in serum, liver, heart and kidneys of goats. 178 40

Alterations in the rat brain carbohydrate and related metabolisms were studied during acute and chronic acephate toxicity. The rats were divided into three batches of eight in each batch. The first batch was treated with chronic (50 mg.Kg-1.day-1 for 7 weeks) and second batch was treated with acute (600 mg.Kg-1.day-1 for one day) doses of acephate, third group was served as control which received vehicle only. The representative enzymes like SDH, MDH, LDH, GDH, AAT and AlAT activities were decreased significantly during chronic treatment. Whereas MDH, LDH, AAT and AlAT activities showed significant increase during acute treatment. The glycogen and pyruvate levels showed nonsignificant elevation and lactate and total carbohydrate levels were depleted in the brains of chronic acephate treated rats. Reverse trend was observed with regard to lactate and pyruvate during acute toxicity whereas the total carbohydrates and glycogen levels were significantly elevated. The decreased oxidative potential and reduced flux of ketoacids into TCA cycle through transamination reactions indicate that acephate caused energy crisis in the brain during chronic treatment. During acute treatment the inhibited succinate oxidation was compensated by the ketoacid contributions through transamination reactions. The neuro transmitter balance with particular reference to glutamate during toxic stress was reflected through the GDH levels in both the treatments.
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PMID:Alterations in glycolytic and oxidative potentials of rat brain during acute and chronic acephate treatments. 195 6

The joint hepatotoxicity of CCl4 and CHCl3 or TCE in male CD rats following simultaneous oral administration has been investigated. Rats with chronic indwelling arterial cannulas were administered a single oral dose of CCl4 and CHCl3 or CCl4 and TCE in 5% Emulphor at doses of 0 to 700 mg/kg. Hepatotoxicity was evaluated by measuring the activity of AST, ALT, and SDH in plasma at 0, 3, 6, 12, 24, 36, 48, and 72 hr postgavage. Response data were analyzed for interaction using response surface methodology. CCl4 alone displayed dose-dependent toxicity. TCE demonstrated little evidence of hepatotoxicity. In combination, both CCl4/CHCl3 and CCl4/TCE displayed a synergistic (supraadditive) response for peak plasma enzyme activity.
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PMID:Interactions of water contaminants. I. Plasma enzyme activity and response surface methodology following gavage administration of CCl4 and CHCl3 or TCE singly and in combination in the rat. 234 Sep 78

To compare the effect of fenbendazole on the liver and liver microsomal mono-oxygenases of goats, quail and rats, an oral dose of 25 mg/kg was administered to the animals daily for 9 consecutive days. On the tenth day, blood samples and livers were collected from both the control and the treated animals for preparation of serum and microsomes respectively. Determination of the activities of sorbitol dehydrogenase (SDH, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum samples showed that there was no significant increase in the activities of these enzymes in the treated animals as compared to their corresponding controls, suggesting no liver damage. Similarly, no significant difference in the amount of microsomal cytochrome P-450 was found between the control and the treated animals of the same species. Compared to their respective controls, the activities of microsomal benzphetamine N-demethylase and aniline hydroxylase were almost unchanged in the treated goats and rats. However, fenbendazole treatment appeared to enhance the activity of these two microsomal enzymes in quail. The results indicate that fenbendazole is not liver toxic to goats, quail or rats at a dose rate of 25 mg/kg.
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PMID:Comparative studies on the effect of fenbendazole on the liver and liver microsomal enzymes in goats, quail and rats. 277 8

To survey the genetic resources of Atlantic salmon (Salmo salar L.) stocks in Finland, an electrophoretic study was made of natural and hatchery stocks. The stocks were compared with the nearest stocks in the USSR, and the effects of hatchery rearing were evaluated. The genetic variation within and between stocks was measured from 20 samples, of which three (Kola, Neva and Onega) were from the USSR. Twenty-five enzyme loci were examined, of which six were polymorphic: AAT-4, IDH-3, ME-3, MDH-3, PGM-1, and SDH-1. The mean heterozygosity of all the populations was 4.2% (1.0-7.2). For the natural salmon stocks of the Arctic Ocean, the mean heterozygosity was 6.3%, for the natural stocks of Atlantic salmon in the Baltic 4.8%, for the hatchery stocks 3.6%, and for the lake salmon (Salmo salar m. sebago Girard) 1.8%. The results are in agreement with the hypothesis that the amount of variation depends on the effective population size and that culture diminishes variation by decreasing the effective population size. All the stocks originating from different rivers differed from each other with statistical significance. The most unique stocks were the River Kola stock and the lake salmon stock from Lake Saimaa. The genetic distances were consistent with the geographic distance between the rivers from which the stocks originated. Stress is laid on the importance in fish culture of maintaining separate stocks and using larger brood stocks.
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PMID:Electrophoretically detectable genetic variation in natural and hatchery stocks of Atlantic salmon in Finland. 277 27

Food intake, plasma and brain amino acid concentrations, liver amino acid catabolic enzyme activities, and whole-brain neurotransmitter and metabolite concentrations were measured in young rats adapted for 11 d to diets containing from 5 to 75% (in increments of 5%) casein. Food intake was depressed initially in rats fed diets containing 5, 10% or greater than 35% casein. For the duration of the experiment, food intakes of the groups fed the higher protein diets improved on successive days; the length and severity of the depression were proportional to the protein content of the diet fed. Rats fed low levels of protein grew poorly, and their food intake remained depressed. The gradual improvement in growth and food intake of rats fed diets containing more than 35% casein was accompanied by dramatic increases in the activities of serine-threonine dehydratase (SDH, EC 4.2.1.16) and glutamate-pyruvate aminotransferase (GPT, EC 2.6.1.1) in liver. The increase in amino acid catabolic activity was accompanied by decreases in the concentrations of most amino acids in plasma and brain. However, concentrations of branched-chain amino acids, in both plasma and brain, increased in direct proportion to the protein concentration of the diet fed. As a result of these reciprocal responses, the total concentration of indispensable amino acids in brain (IAA) was maintained within a narrow range of values, despite a sixfold range of protein intakes. Whole-brain concentrations of norepinephrine, dopamine and serotonin were not correlated with dietary protein concentration, total food intake or protein intake. Brain concentrations of homovanillic acid and 5-hydroxyindoleacetic acid were correlated inversely with protein intake and that of 3,4-dihydroxyphenylacetic acid was correlated directly with food intake. Protein intake appeared to be related to the animal's ability to maintain brain total IAA content between some upper and lower limits. Our results indicate that this was accomplished initially through downward adjustment of protein intake and subsequently through an increase in catabolic capacity for the amino acids.
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PMID:Adaptation of rats to diets containing different levels of protein: effects on food intake, plasma and brain amino acid concentrations and brain neurotransmitter metabolism. 285 80


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