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Lipid peroxidation in purified plasma membrane fractions of rat liver in relation to the hepatoxicity of carbon tetrachloride
Author(s) -
Le Page R. N.,
Cheeseman K. H.,
Osman N.,
Slater T. F.
Publication year - 1988
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290060203
Subject(s) - lipid peroxidation , chemistry , microsome , carbon tetrachloride , membrane , biochemistry , endoplasmic reticulum , hepatocyte , enzyme , in vitro , organic chemistry
Preparations of rat liver sinusoidal plasma membrane have been tested for their ability to metabolize the hepatotoxin carbon tetrachloride (CCl 4 ) to reactive free radicals in vitro and compared in this respect with standard preparations of rat liver microsomes. The sinusoidal plasma membranes were relatively free of endoplasmic reticulum‐associated activities such as the enzymes of the cytochrome P 450 system and glucose‐6‐phosphatase. CCl 4 metabolism was measured as (i) covalent binding of [ 14 C]‐CCl 4 to membrane protein, (ii) electron spin resonance spin‐trapping of CCl 3 · radicals and (iii) CCl 4 ‐induced lipid peroxidation. By all of these tests, purified sinusoidal plasma membranes were found unable to metabolize CCl 4 . The fatty acid composition of the plasma membranes was almost identical to that of the microsomal preparation and both membrane fractions exhibited similar rates of the lipid peroxidation that was stimulated non‐enzymically by γ‐radiation or incubation with ascorbate and iron. The absence of CCl 4 ‐induced lipid peroxidation in the plasma membranes seems to be due, therefore, to an absence of CCl 4 activation rather than an inherent resistance to lipid peroxidation. We conclude that damage to the hepatocyte plasma membrane during CCl 4 intoxication is not due to a significant local activation of CCl 4 to CCl 3 · within that membrane.