Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.2.13 (aldolase)
3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of bovine somatotropin in acute CCl4 poisoning was studied in rabbits. Somatotropin was injected subcutaneously in doses of 2.5 mg/kg. Liver damage was assessed on the basis of alanine and aspartate aminotransferase and aldolase activities. STH injected during 10 experimental days or 5 days preceding experimental poisoning with CCl4 did not increase the degree of liver damage in comparison with the group of animals injected only with carbon tetrachloride.
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PMID:Influence of bovine somatotropin on the liver experimentally damaged with carbon tetrachloride. 116 53

The enzymic tests and radionuclide hepatography were used to study and compare liver function after rabbits were exposed to tetrachloromethane poisoning. The activity of serum enzymes of cholinesterase, alkaline phosphatase, aldolase and leucine aminopeptidase was determined. Hepatography was made with the use of 198Au-colloid with an activity 0.74 MBC. The enzymic tests were demonstrated to be more sensitive than radionuclide hepatography in detecting the earliest parenchymatous lesions in the liver. The data obtained correlate with the data of the pathohistological examinations, which demonstrated the presence of marked vacuole parenchymatous fatty dystrophy. The authors recommend that the enzymic tests should be used for detecting early hepatic lesions induced by tetrachloromethane.
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PMID:[Potentials of enzyme tests and radioisotope hepatography in detecting early functional changes in the liver]. 298 74

Level of fructose-1-monophosphate aldolase was decreased in blood serum after administration of phosphatidyl choline-containing liposomes into male rats with experimental toxic hepatitis caused by treatment with hepatotropic poison CCl4 at a dose of 0.25 ml/100 g of body mass. The rate of the aldolase level normalization depends on composition of liposomes as well as on the pathway of their administration.
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PMID:[Protective effect of phosphatidylcholine liposomes in experimental toxic hepatitis]. 372 72

The authors performed a comparative biochemical study of some enzymes of lysosomic origin (hyaluronidase, N-acetyl-beta-D-glucosaminidase, beta-glucosidase, beta-galatosidase and acid phosphatase), of the state of enzyme substrate system N-acetylneuraminic acid---aldolase of neuramic acid and of the activity of lactatedehydrogenase (soluble in cytosol and bound on mitochodria) in the liver, lungs and blood serum of rats at various regimens of the inhalation action of CCl4. On the basis of results obtained they determined the biological importance of the change of activity of enzymes differently localized in cells at the adaptation of an organisme to the noxious action of CCl4.
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PMID:The influence of tetrachloromethane on subcellular structures of rat hepatocyte lysosomal and cytoplasmic enzymes of the liver, lungs and blood serum of rats during continuous and intermittent action of tetrachloromethane. 719 Sep 85

The hepatic response to a fructose challenge for control rats, and rats subjected to an acute sublethal dose of carbon tetrachloride (CCl4) or bromobenzene (BB), was compared using dynamic in vivo 31P MRS. Fructose loading conditions were used in which control rats showed only a modest increase in hepatic phosphomonoester (PME), and a small decrease in ATP, Pi, and intracellular pH after fructose administration. Both CCl4 and BB-treated rats showed a much greater fructose-induced accumulation of PME than did controls. Trolox C, a free radical scavenger, prevented most of this PME increase. BB-treated rats, given sufficient time to recover from the hepatotoxic insult, responded to the fructose load similarly to controls. Liver aldolase activities of control, toxicant-treated rats, and toxicant plus Trolox C-treated rats correlated inversely with PME accumulation after fructose loading (correlation coefficient: -0.834, P < 0.05). Perchloric acid extracts of rat livers studied by in vitro 31P MRS confirmed that the PME accumulation after fructose loading is mainly due to an increase in fructose 1-phosphate. These studies are consistent with the aldolase-catalyzed cleavage of fructose 1-phosphate being rate-limiting in hepatic fructose metabolism, and that the CCl4 and BB treatment modify and inactivate the aldolase enzyme.
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PMID:In vivo and in vitro 31P magnetic resonance spectroscopic studies of the hepatic response of healthy rats and rats with acute hepatic damage to fructose loading. 786 5