Two mechanisms of CCl4-induced fatty liver: lipid peroxidation or covalent binding studied in cultured rat hepatocytes.
With cultured hepatocytes it was studied whether CCl4-induced inhibition of secretion of VLDL and HDL from liver cells is a consequence of covalent binding of CCl4 metabolites (i.e. CCl3; CCl3OO.) to cell constituents or of membrane damage by lipid peroxidation. Comparing the kinetics of inhibition of lipoprotein secretion with that of CCl4-bioactivation it was found, that covalent binding of (14C)-CCl4 occurred at early time points (5 min) after CCl4 administration and inhibited the lipoprotein secretion. At 100 microM CCl4 it was depressed by 53% within 60 min. Incubations of CCl4-treated cells with increasing concentrations of vitamin E blocked lipid peroxidation, but lipoprotein secretion was still inhibited. Piperonyl butoxid, a radical scavenger, protected against CCl4-induced inhibition of lipoprotein section, lipid peroxidation and covalent binding. These results show that during the early phases of CCl4 poisoning fat accumulation is the consequence of covalent binding of CCl4 metabolites to cell structures.[1]References
- Two mechanisms of CCl4-induced fatty liver: lipid peroxidation or covalent binding studied in cultured rat hepatocytes. Becker, E., Messner, B., Berndt, J. Free Radic. Res. Commun. (1987) [Pubmed]
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