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 purpose of our investigation was to study the effect of somatostatin on acute experimental liver injury induced in rats by galactosamine (1.2 g/100 g body wt.). Somatostatin (125 micrograms/100 g body wt.) was administered subcutaneously in a protamine sulphate/ZnCl2 suspension either 2 h prior to the injection of galactosamine or 2 h and again 12 h following the injection. Serum transaminases (GOT, GPT) and serum concentrations of triiodothyronine and thyroxine were determined 28 h after the injection of galactosamine. Histology of the liver was performed by light microscopy. Our results showed that the administration of somatostatin significantly (P less than 0.02) reduced the elevation of GOT and GPT activity and diminished the degree of necrosis, and that although the administration of dibutyryl-cAMP (5 mg/100 g body wt.) intensified galactosamine induced liver injury, this effect of dibutyryl-cAMP could be completely prevented by somatostatin treatment. There was no difference in the serum concentrations of triiodothyronine and thyroxine in controls as compared to galactosamine and galactosamine plus somatostatin treated rats. At present the mechanism of this cytoprotection by somatostatin is unknown.
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PMID:Beneficial effect of somatostatin on galactosamine induced liver injury. 614 23

H2 receptor antagonist-hepatotoxicant interactions were evaluated in male Fischer-344 rats. The H2 receptor antagonists, cimetidine, ranitidine, oxmetidine, and 2-[2-(2-dimethyl-aminomethyl-5-furanylmethyl-thio)-ethylamino]-5-( 6-methyl- 3-picolyl)-4-pyrimidine trihydrohydrochloride (SK&F 93479) were administered (p.o.) at a dose of 0.143 mMoles/kg 30 minutes prior to hepatotoxicant treatment. Submaximal hepatotoxic doses (p.o.) of carbon tetrachloride (795 mg/kg), bromobenzene (748 mg/kg), chloroform (1,190 mg/kg), allyl alcohol (60 mg/kg), galactosamine (200 mg/kg, i.p.), and acetaminophen (1000 mg/kg) were employed. Hepatotoxicity was evaluated by determining serum alanine aminotransferase activity (ALT). Pretreatment with the H2 receptor antagonists did not significantly alter carbon tetrachloride or allyl alcohol hepatotoxicity. Bromobenzene and chloroform toxicities were unaffected by cimetidine, ranitidine, and oxmetidine pretreatment but were potentiated by SK&F 93479. Cimetidine and ranitidine decreased galactosamine mediated hepatotoxicity. Acetaminophen hepatotoxicity was markedly potentiated by ranitidine pretreatment but was unaltered by the other three H2 receptor antagonists. The mechanisms of hepatotoxicity potentiation or protection have not been determined, however, the lack of consistent H2 receptor antagonists effects indicates that it is unlikely that alterations in G.I. pH account for the effects observed. H2 receptor antagonist mediated changes in hepatotoxicant metabolism provide a more plausible mechanism of action, particularly in the cases of SK&F 93479 potentiation of bromobenzene and chloroform and ranitidine potentiation of acetaminophen hepatotoxicity.
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PMID:Effects of H2 receptor antagonists on the hepatotoxicity of various chemicals. 614 1

Female rats treated with D-galactosamine showed increased serum enzyme levels of lactate dehydrogenase, alanine transaminase and sorbitol dehydrogenase as well as moderately elevated liver calcium and decreased potassium contents 4 and 8 hours after drug administration. Slightly but significantly more calcium was sequestered in the liver when the animals were additionally pretreated with vitamin D3, while the other investigated factors were not altered by this treatment. A different pattern was found in carbon-tetrachloride-induced liver lesion. Liver calcium levels were also raised when animals with carbon tetrachloride were pretreated with vitamin D3, but in contrast to D-galactosamine injury, liver enzyme release and electrolyte shift were markedly inhibited under these conditions. Together with previously reported results these findings support our concept that an early rise in liver cell calcium content with a related protective effect is a specific phenomenon in carbon-tetrachloride-induced liver cell damage.
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PMID:The role of calcium in liver cell damage. Comparative studies with carbon tetrachloride and D-galactosamine. 626 Dec 29

After administration of D-galactosamine-HCl alterations in liver cells - histologically resembling hepatitis - occur. During this process several biochemical changes are demonstrable. The formation of these alterations may be prevented by combined administration of nicotinamide + L-methionine or DL-tryptophan + L-methionine. This had been confirmed by histology as well as by determination of GOT and GPT activity in the serum.
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PMID:The influence of nicotinamide, tryptophan, and methionine upon galactosamine-induced effects in the liver. 645 26

The possible protective effect of cysteine on chemical-induced liver injury was studied in rats in vivo and in vitro. There was no increase in the activity of serum glutamic oxaloacetic transaminase (GOT) of rats pretreated with cysteine (1.2 g/kg, p,o.) followed by 0.25 ml/kg carbon tetrachloride (CCl4), d-galactosamine (GalN) or alpha-naphthylisothiocyanate (ANIT). However, rats pretreated with cysteine followed by 0.5 ml/kg CCl4 were not protected. The content of cytochrome P-450, activity of aminopyrine N-demethylase or serum ratio of 5,5-dimethyl-2,4-oxazolidinedione (DMO) to trimethadione (TMO) (DMO/TMO ratio) after CCl4, GalN or ANIT were not altered by pretreatment with cysteine. However, pretreatment with cysteine prevented changes in the content of cytochrome P-450, activity of aminopyrine N-demethylase and DMO/TMO ratio in serum as well as the activities of serum GOT and GPT when the rats were treated with bromobenzene (BZ). The degree of lipid peroxidation from CCl4 was markedly reduced by the presence of 10(-4)M cysteine. These results suggest that cysteine has a protective effect on chemical-induced liver injury produced via epoxide metabolites.
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PMID:The protective effect of cysteine on chemical-induced liver injury in rats. 650 63

Severity of liver damage 24 hr after i.p. administration of carbon tetrachloride (0.2 ml/kg), allyl alcohol (0.036 ml/kg) or galactosamine (400 mg/kg) was evaluated in male rats at 4-5, 14-15 or 24-25 months of age. Allyl alcohol hepatotoxicity, as judged by light microscopy and serum alanine aminotransferase levels, increased markedly as a function of age. In contrast, carbon tetrachloride and galactosamine toxicities were unchanged or slightly diminished in old rats. Hepatic glutathione (GSH) concentrations were unaffected by aging; thus, the age-dependent increase in susceptibility to allyl alcohol toxicity was not a result of diminished GSH availability in old age. Hepatotoxicant-induced changes in GSH were observed in allyl alcohol-treated old rats (20% increase) and in galactosamine-treated young-adult and middle-aged rats (30% decrease).
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PMID:Effect of aging on liver glutathione levels and hepatocellular injury from carbon tetrachloride, allyl alcohol or galactosamine. 653 34

The effects of allyl alcohol, galactosamine, bromobenzene, and corn oil administration were evaluated in male Fischer 344 rats at 4 to 5, 14 to 15, and 24 to 25 months of age to determine if susceptibility to hepatotoxic injury is modified as a consequence of aging. Parameters measured were (1) severity of hepatocellular necrosis as judged by light microscopy of liver sections, (2) activity of alanine aminotransferase and aspartate aminotransferase in serum, and (3) hepatic microsomal cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity. Allyl alcohol toxicity was more severe in middle-aged and old rats than in young-adult rats. In contrast, galactosamine and bromobenzene toxicities were slightly decreased or unchanged in old rats. The results demonstrate that aging has effects on some types of chemically induced hepatotoxicity.
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PMID:Influence of aging on the susceptibility of rats to hepatotoxic injury. 671 May 24

The biochemical and morphological effects of 2, 10 and 100 mM of D-galactosamine (GalN) were studied in isolated rat hepatocytes during 2 h of incubation. Lactate dehydrogenase (LDH), alanine aminotransferase (ALAT) and cell viability did not change, whatever the concentration used. The variations observed, which were dose dependent, included a large drop in ATP levels and inhibition of RNA and protein synthesis. A very high concentration of GalN was necessary, however, to induce a significant decline in methionine adenosyltransferase activity compared to control cells. The use of L-[methyl-14C]methionine during cell incubation with GalN demonstrated a decrease of S-adenosyl-L-methionine (SAMe) and an accumulation of L-methionine content related to the GalN concentration. These results suggested that an hepatotoxic agent such as GalN was able to induce disturbances of methionine metabolism. Some of the ultrastructural changes observed were different from those previously found in vivo, in rats given GalN intraperitoneally, underlining the marked difference between in vivo and in vitro intoxication.
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PMID:Methionine metabolism and ultrastructural changes with D-galactosamine in isolated rat hepatocytes. 674 76

Studies by Liehr et al. suggest that endotoxins are important in the pathogenesis of galactosamine hepatitis (Gal-N hepatitis) in rats. Lactulose (9.1 gm per kg per day) prevents hepatic lesions induced by Gal-N; an antiendotoxin effect of lactulose is postulated. However, commercial preparations of lactulose are contaminated with galactose, which shows a competitive action to Gal-N. To analyze the effect of galactose, male Wistar rats were pretreated with lactulose (Duphalac, 9.1 gm per kg per day) and given Gal-N (375 mg per kg i.p.). After 24 hr, serum was analyzed for glutamic pyruvate transaminase, glutamate dehydrogenase, and sorbitol dehydrogenase activities. Pretreatment with Duphalac, even 1 hr before Gal-N, abolished toxicity. Duphalac contains 10 gm galactose per 100 ml. Galactose was given in a similar concentration and similar inhibition occurred. Pretreatment with purified lactulose (9.1 gm per kg for 5 days) diminished the effects of Gal-N but did not normalize enzyme concentrations. Because small doses of galactose (80 and 300 mg per kg) showed similar inhibitory effects, we conclude that the protective effect of commercial lactulose preparations is mainly due to galactose contamination and not to an antiendotoxin effect.
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PMID:Galactosamine hepatitis, endotoxemia, and lactulose. 683 15

The hepatoprotective effect of carsil (generic name silymarin) on a model of liver intoxication with D-galactosamine in rats is studied. The changes in the activity of the serum enzymes GOT, GPT, MDH, SDH, ICDH, AP. AhE and the total protein as well as the UDP-sugars content in the liver is investigated. Histochemical and electronmicroscopical investigations of the liver are carried out simultaneously. It is obvious that carsil prevents to a considerable degree the increase of the serum enzymes activity caused by a D-galactosamine injury, enhances the metabolic conversion of the UDP-hexosamine into UDP-acetylhexosamine in the liver and hastens the normalizing of the UDP-glucuronic acid content in the liver of rats. The biochemical and morphological changes under the influence of carsil and the possible biochemical mechanism of the drug action is discussed.
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PMID:Hepatoprotective effect of silymarin (carsil) on liver of D-galactosamine treated rats. Biochemical and morphological investigations. 723 Sep 79


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