Lipid Peroxidation and Haloalkylation in CCl4-Induced Liver Fatty Degeneration and Necrosis
Liver fatty accumulation following acute CCl4 poisoning is triggered by a block of lipoprotein secretion which occurs very soon after treatment.1,2 Various steps of the secretory pathway are probably involved in the expression of such damage. Recent studies with isolated rat hepatocytes have shown a marked impairment of the maturation and transport of lipoprotein micelles at the level of the Golgi apparatus soon after poisoning with CCl4.3. In the present paper the demonstration of early disturbances of liver Golgi function occurring in the whole animal dosed with CCl4 is reported, together with studies on the pathogenesis of this cellular perturbation. In addition, the relative role played by CCl4-dependent alkylation of macromolecules and lipid peroxidation in the necrogenic effect of the toxin has been evaluated in in vivo experiments.
KeywordsCarbon Tetrachloride Lipoprotein Secretion Cellular Perturbation Golgi Fraction CCi4 Group
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