Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fructose, proteins, and glutamic oxalacetic and pyruvic transaminases (GOT and GPT) were measured in the saminal plasma in a group of 20 normal males, 30-40 years old, subjected to vasectomy. The differences between the values obtained before and 6 months after the vasectomy were statistically insignificant. Therefore, it is concluded that the androgenic function of the testis is unaffected by the bilatera l occlusion of the vas deferens, and that certain enzymes, such as GOT a nd GPT, are incorporated in the semen by the prostate and/or by the seminal vesicles, rather than by the testis. The study reports for the 1st time the average concentrations of GPT in the seminal plasma of normal subjects.
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PMID:[Determination of fructose, proteins, oxalacetic and pyruvic transaminase in the seminal plasma of vasectomized patients]. 94 98

A controlled clinical trial comparing 2-Mercapto-Priopionyl-Glycine (2-MPG) plus B12 vitamin with B12 vitamin alone in chronic liver disease has been conducted in seven hospitals in Italy. Patients were divided into two groups on the basis of liver histology; group I included 26 patients showing histological evidence for chronic persistent hepatitis (C.P.H.) (according to De Groote et al.) whereas group II consisted of 54 patients with chronic aggressive hepatitis (C.A.H.) or compensated liver cirrhosis. Patients of each group were randomly allocated to 2-MPG plus B12 vitamin, or to placebo plus B12 vitamin, in a double-blind way. The drug (or placebo) was diluted in 500 ml of 10% Levulose, and administered intravenously; 1000 gamma of B12 vitamin were added to each bottle. Patients in the 2-MPG group received 2.5 gms of the drug daily; the treatment lasted for 30 days. The following parameters were checked in all patients on admission, and repeated at the end of treatment: Serum bilirubin, serum Cholesterol, A.P., BSP retention, Prothrombin time, S-GOT, S-GPT, Gamma-GT, Total serum Protein, serum electrophoresis, Immunoglobulins. Patients given 2-MPG showed significant decreases of serum transaminases, and improvement of BSP retention.
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PMID:[Controlled clinical trial of 2-mercapto-propionyl-glycine in chronic hepatopathies]. 125 87

Using rat hepatocytes we confirmed our previous results that glucagon and beta-adrenergic agonists increased the enzyme activity of alanine aminotransferase (AAT) and propranolol abolished their effects. Only the enzyme activity was measured and other parameters like quantity of the enzyme or activation due to modification were not looked for. As in perfusion experiment phenylephrine and phenoxybenzamine (alpha-agonist and alpha-antagonist respectively) also alpha-antagonist respectively) also increased the AAT activity in isolated rat hepatocytes and propranolol reversed these effects. The additive effect of glucagon and phenoxybenzamine on AAT was also persistent in hepatocyte system. Fructose-1:6-bisphosphatase (Fru-P2-ase), another key enzyme in gluconeogenic pathway, was elevated by glucagon and other beta-adrenergic agonists both in liver perfusion and isolated hepatocyte experiments and was brought back to the normal level by propranolol. In this case also only the enzyme activity was measured and no other parameters were looked for. Unlike AAT this enzyme was not stimulated by phenylephrine or phenoxybenzamine. But AAT and Fru-P2-ase activities were increased significantly by adenylate cyclase activators like fluoride or forskolin. Thus, it appears that the regulation of fru-P2-ase by glucagon is purely a b-receptor mediated process whereas AAT activation shows a mixed type of regulation where some well known alpha-agonist and antagonists are behaving as beta-agonists. Results further indicate the presence of phosphodiesterase in hepatocyte membrane which was stimulated by glucagon and brought back to the normal level by propranolol. The different adrenergic compounds stated above, not only modified the activity of the above two enzymes but also stimulated glucose production by hepatocytes from alanine which was in turn abolished by propranolol as well as amino oxyacetate (AOA), a highly specified inhibitor of AAT. This confirm the participation of AAT in gluconeogenesis from alanine in liver. Forskolin and fluoride also increased the glucose production from alanine and showed additive effects with glucagon, phenylephrine and phenoxybenzamine.
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PMID:Effect of adrenergic agonists and antagonists on alanine amino transferase, fructose-1:6-bisphosphatase and glucose production in hepatocytes. 135 93

1. Adult, female Xenopus laevis were subjected to 12 months of starvation. 2. Starvation resulted in a continuous reduction in the activity of both hepatic and renal glucose-6-phosphate dehydrogenase. 3. Fructose-1,6-diphosphatase was significantly reduced at months 10 and 12 in the liver, and at months 4, 10, and 12 in the kidney. 4. Pyruvate kinase activity of muscle and liver decreased during the experimental period whereas the renal enzyme remained essentially unchanged. 5. Both hepatic and renal glutamate-pyruvate transaminase (GPT) and hepatic glutamate-oxaloacetate transaminase (GOT) showed a reduction of activity after 2 and 4 months of starvation followed by an increase in GPT but not in GOT.
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PMID:Long-term starvation in Xenopus laevis Daudin--III. Effects on enzymes in several tissues. 255 3

Livers of starved rats refed for 2 h were perfused in situ by a modification of the dual digitonin pulse technique of Quistorff and Grunnet (Quistorff, B., and Grunnet, N. (1987) Biochem. J. 243, 87-95). A pulse of digitonin (2 mg/ml) was infused first antegrade through the portal vein followed retrograde through the vena cava, or in reverse order, 13 mg of digitonin per zone. Microscopic examination showed that this procedure permeabilized the periportal and perivenous zones of the liver without overlap, with a narrow unaffected band of hepatocytes between the zones. The distribution pattern between periportal and perivenous zones ratio for alanine transaminase, lactate hydrogenase, fructose-1,6-bisphosphatase, and phosphoenolpyruvate carboxykinase ranged from 1.5 to 3. Glucokinase activity was higher in the perivenous zone (periportal/perivenous ratio of 0.7) and glutamine synthetase was exclusively present in that zone. Fructose 2,6-bisphosphate concentration was nearly equal in the two zones.
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PMID:The zonation of liver and the distribution of fructose 2,6-bisphosphate in rat liver. 289 7

The effect of 90% jejunoileal bypass procedure on liver enzymes was evaluated in 11 obese Zucker fat rats after a 50% weight loss. Control tissues were also collected from 11 unoperated obese rats. In the jejunoileal bypass group, there was a significant decrease in phosphofructokinase, pyruvate kinase, and glucose-6-phosphate dehydrogenase activities. Pyruvate carboxylase, alanine aminotransferase, and lactate dehydrogenase activities were not altered. Fructose 1,6-biphosphatase, aldolase, aspartate aminotransferase, and phosphoenolpyruvate carboxykinase activities were increased in the jejunoileal bypass group. These studies suggest that after jejunoileal bypass glycolysis is reduced and gluconeogenesis is increased. Amino acids may provide an essential energy source for hepatic function.
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PMID:Changes in hepatic carbohydrate metabolism after jejunoileal bypass. 707 18

Suspensions of isolated rat hepatocytes incubated in the presence of the diabetogenic agent alloxan exhibit time- and concentration-dependent damage. At concentrations of 3.5 mM and above, alloxan caused an increase in lactate dehydrogenase (LDH), glutamate-pyruvate transaminase (GPT) and intracellular potassium (K+) leakage, all of which are indices of plasma membrane damage, and decreased the intracellular reduced glutathione content (GSH) of the cells. Preincubation (10 min) in D-glucose (50 or 100 mM, but not 10 mM) partially protected the hepatocytes from LDH, GPT and K+ leakage and the decrease in GSH produced by alloxan (7 mM) during a 60-min incubation period. Other sugars (D-galactose, 2-deoxy-D-glucose, D-fructose, D-mannoheptulose and D-mannitol) were also found to protect hepatocytes against damage caused by alloxan. D-Fructose was found to be the most potent protective sugar. These results indicate that alloxan is not selectively toxic to the pancreatic beta-cell and that sugars can protect against alloxan-induced cytotoxicity in hepatocytes.
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PMID:Alloxan toxicity in isolated rat hepatocytes and protection by sugars. 715 55

1. Although oral administration of 400 mg/kg acetaminophen (APAP) or 1.8-3.4 g/kg sucrose had no effect on serum levels of alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH), their co-administration resulted in 20-fold increases in ALT/SDH activities. APAP alone (1250 mg/kg, p.o.) caused the elevation hepatotoxicity parameters, but the levels were lower than observed with co-administration of APAP (400 mg/kg) and sucrose (2.6 or 3.4 g/kg). 2. Sucrose-associated increase in serum ALT/SDH activities was selective with APAP and not detected with carbon tetrachloride (160 mg/kg, i.p.), D-galactosamine (400 mg/kg, i.p.) or alpha-naphthyl isothiocyanate (100 mg/kg, p.o.). 3. To verify the synergistic mechanism of sucrose, a major reactive intermediate of APAP, N-acetyl-p-benzoquinone imine (NAPQI), was given via the portal vein to rat pretreated with sucrose. Clear elevation of ALT/SDH activities was detected in the co-treated group. These results, together with an allopurinol-inhibition experiment, suggest the involvement of high-dose sucrose at a step(s) occurring after the metabolic activation of APAP. 4. Co-administration of glucose or fructose as well as sucrose elevated APAP-induced hepatotoxicity parameters in rat. Fructose but not glucose elevated APAP- or NAPQI-induced LDH leakage in a primary hepatocyte system. The results suggest the primary role of fructose is on the sucrose enhancement of APAP toxicity in rat.
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PMID:Hepatotoxicity of acetaminophen and N-acetyl-p-benzoquinone imine and enhancement by fructose. 1105 70

Fructose-1,6-bisphosphate (FBP) has been reported to have a protective effect on liver injury following ischemic/reperfusion periods. FBP maintains ATP levels and thereby cellular energy metabolism, which is important to the liver during cold preservation. In the present study, we evaluated the effects of FBP on the composition of storage solutions for cold liver preservation. Adult male Wistar rats were randomly divided into three experimental groups. Hepatic perfusion and preservation were performed with UW, UW plus 10 mmol/L FBP (UWM), and FBP 10 mmol/L (FBPS) alone solutions. Biochemical measurements of AST, ALT, and TBARS were performed on samples of the cold storage solution at 0, 12, 18, and 24 hours preservation. FBPS and UW solutions showed similar preservation grades during 18 hours. Addition of 10 mmol/L of FBP to UW solution induced liver injury and a poor preservation grade. FBP appears to protect the liver from injury caused by free radicals when the preservation time is less than 18 hours. Therefore, FBP may exert a protective effect for the preservation of livers during cold storage, and could represent an important component of new cold storage solutions.
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PMID:Protective effect of fructose-1,6-bisphosphate in the cold storage solution for liver preservation in rat hepatic transplantation. 1525 7

Fructose-1,6-bisphosphate (FBP) has been reported to have a protective effect on liver injury following ischemic/reperfusion periods because it maintains ATP levels during cold preservation. In the present study, we evaluated the effects of addition of FBP to storage solutions for cold liver preservation during 12 or 36 hours. Adult male Wistar rats were randomly divided into three experimental groups. The hepatic perfusion and preservation were performed with these solutions: UW; UW plus 10 mmol/L FBP; and FBP 10 mmol/L (FBPS) alone. The biochemical measurements of AST and ALT were performed on samples of the cold storage solution after 12- or 36-hour preservation. UW and FBPS solutions showed similar preservation grades at 12 hours. Addition of 10 mmol/L of FBP to UW solution induced liver injury and a poor preservation grade during 12 or 36 hours. UW solution was better than FBPS after 36 hours preservation. UW solution continues to offer a superior performance for liver preservation during long times; however, FBPS may be an alternative for short cold preservation times.
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PMID:Effect of fructose-1,6-bisphosphate in the cold storage solution after 12 and 36 hours of rat liver preservation. 1562 Oct 98


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