Abstract
The role of the oxygen radicals in lipid peroxidation, induced by ADP/Fe 3+ or cumene hydroperoxide was investigated by administering diethyldithiocarbamate, an inhibitor of Superoxide dismutase, to hepatocytes or rats. Intact rat-liver hepatocytes perform a delayed ADP/Fe 3+-induced lipid peroxidation after pretreatment with diethyldithiocarbamate. The cumene hydroperoxide-induced lipid peroxidation is unchanged. Hepatocytes, isolated from a rat administered with diethyldithiocarbamate in vivo, exhibit the same pattern, a delayed iron-induced lipid peroxidation and an unchanged cumene hydroperoxide-induced lipid peroxidation. Liver microsomes isolated from liver of a rat administered with diethyldithiocarbamate do not perform lipid peroxidation with NADPH/ADP/Fe 3+, but do undergo lipid peroxidation with cumene hydroperoxide. It can be concluded that besides the inhibition of Superoxide dimutase, diethyldithiocarbamate inhibits directly the microsomal lipid peroxidation. Although this inhibition hampers the conclusion, evidence is obtained that Superoxide dismutase is probably involved in the protection against lipid peroxidation of the mitochondria, but not of the microsomes.
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