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Liver biopsies from 9 out of every 10 obese individuals exhibit pathological changes of unknown aetiology and 3 out of every 10 reflect severe injury in the form of periportal fibrosis. To examine the hypothesis that excessive fibrosis in obesity arises in part from a predisposition to injury of the
The cellular kinetics of repair and scarring which occurs after induction of periportal necrosis in mice by allyl alcohol were examined by histology and immunohistochemistry. Thirty-six six-week-old female C57BI/6J mice were injected intraperitoneally with two doses of allyl alcohol on day 0 and
The prevention of liver damage in rats intoxicated with allyl alcohol was attempted with 5 per cent Ca--Mg gluconolactate in reiterated doses. This preparation prevented or reduced liver necrosis only in the presence of spleen: splenectomy annihilated the effect of Ca--Mg gluconolactate.
To determine the involvement of different hepatocyte populations in response to periportal injury, the restitutive response to allyl alcohol (AA) injury was examined. Adult female Sprague-Dawley rats were injected intraperitoneally (IP) with 0.62 mmol/kg AA, killed at 6, 9, 12, 33, 57, 81, and 153
The ultrastructural characteristics of the putative liver stem cells that repopulate the necrotic periportal zones after allyl alcohol induced liver injury are described. Periportal liver cell necrosis was induced in adult female Sprague-Dawley rats by i.p. injection with 0.62 mmol/kg of allyl
The role of iron in allyl alcohol-induced lipid peroxidation and hepatic necrosis was investigated in male NMRI mice in vivo. Ferrous sulfate (0.36 mmol/kg) or a low dose of ally alcohol (0.6 mmol/kg) itself caused only minor lipid peroxidation and injury to the liver within 1 h. When FeSO4 was
Allyl acetate, allyl alcohol, and acrolein are used in the manufacture of detergents, plastics, pharmaceuticals, and chemicals and as agricultural agents and food additives. Male and female F344/N rats and B6C3F(1) mice received allyl acetate, allyl alcohol, or acrolein by gavage for 14 weeks.
BACKGROUND
Some of the biochemical events that lead to necrosis of the liver are well-known. However, the pathogenesis of necrosis of the liver from exposure to hepatotoxicants is a complex biological response to the injury. We hypothesize that gene expression profiles can serve as a signature to
Within 24 h after administration of allyl alcohol the livers showed periportal necrosis and elevation of hepatic glutathione. After 48 h no necrosis was observed in spite of level of hepatic glutathione. The relationship between the hepatic glutathione and liver regeneration is discussed.