The data available in literature concerning the induction of lipid peroxidation (LP) with chronic alcohol administration are systematized. LP can be considered as one of the main processes leading to cellular membrane damage. The cytotoxic activity is attributed not only to the free radicals but also to the final products of the lipid hydroperoxide decomposition, such as malonic dialdehyde and 4-hydroxyalkenals. Data about antioxidative defence enzymes (glutathione peroxidase and transferase, catalase superoxide dismutase) and less investigated protein factors which inhibit LP are summarized; particular attention is paid to changes in their activity during chronic alcoholization. Molecular mechanisms underlying the LP stimulation in the liver tissue against a background of ethanol ingestion are analyzed. New data are presented on the role of peroxisomes in the development of alcohol cardiomyopathy.