[Intravenous infusion of carbohydrate after induction of acute hepatic injury by CCl4 and its effect on injured liver (author's transl)].
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Animals↗
Biomedical subjects
H Aoe
Publications and source records attributed to H Aoe.
Undifferentiated patterns of key carbohydrate-metabolizing enzymes in injured livers. I. Acute carbon-tetrachloride intoxication of rat.
In acute CCL4 intoxication of rats significantly increased activities of hepatic low-Km hexokinases, glucose-6-phosphate dehydrogenase, phosphofructokinase, aldolase A and pyruvate kinase M2 with concurrently decreased activities of glucokinase, glucose-6-phosphatase, fructose-1,6-diphosphatase, aldolase B and pyruvate kinase L were observed. The resulting enzyme pattern was apparently different from that in dietary induction. Principal component analysis revealed that the degree of enzyme deviation in the injured liver was much greater than that in the regenerating liver after partial hepatectomy and was closer to that in fetal liver or hepatoma tissue.
Adenosine Monophosphate↗
[Changes in the activities of rate-limiting enzymes of carbohydrate metabolism in the liver during disturbances of hepatic circulation--with special reference to changes associated with portal ligation].
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Animals↗
Development of hepatocellular carcinomas in rats treated with benzene hexachloride.
The effects of prolonged oral administration of the alpha-, beta-, and gamma-isomers of benzene hexachloride (BHC) on rat liver were examined histologically. Well-differentiated hepatocellular carcinomas were observed in the liver of rats fed a basal diet containing 1,500 or 1,000 parts per million (ppm) of alpha-BHC for 72 weeks. Many typical nodular hyperplasias developed in all groups given 1,500 or 1,000 ppm alpha-BHC. In non-neoplastic areas, slight oval cell infiltration and bile duct proliferation were seen. No neoplastic changes or other abnormal findings, such as oval cell infiltration, fatty changes, fibrosis, or bile duct proliferation of the liver, were observed in groups receiving 500 ppm alpha-, beta-, gamma-, or gamma-BHC.
Administration, Oral↗
Effect of various factors on induction of liver tumors in animals by the alpha-isomer of benzene hexachloride.
The tumorigenic effect of a diet containing the alpha-isomer of benzene hexachloride (alpha-BHC) on the liver of various animals was examined. It was found that alpha-BHC induced liver tumors in male and female mice but not in rats or hamsters in the present observations. Histological changes in the liver of mice induced by alpha-BHC were also much greater than those induced in rats or hamsters. Male animals were more susceptible to the tumorigenic action of alpha-BHC than females. Among different strains of mice, the DDY showed greatest susceptibility and the C57BL/6 showed the least. Induction oflpha-BHC was not inhibited by concomitant feeding of 1-naphthyl isothiocyanate or p- hydroxypropiophenone. However, 3-methylcholanthrene slightly inhibited their induction by alpha-BHC.
Animals↗