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Accumulation of malondialdehyde in mouse heart following acute dosing with adriamycin is strain specific and unaffected by cardiac catalase status.

CDF1 and C57BL/6J male mice were acutely dosed with Adriamycin (ADR), and total cardiac malondialdehyde (MDA) quantitated following isolation by modification of previously developed procedures. Cardiac MDA content in CDF1 mice increased significantly 5 days following ADR dosing as reported by others, but was unchanged in C57BL/6J mice. ADR-induced mortality and a significant loss in cardiac weight 2-3 days after treatment was similar in both strains. Cardiac lipid hydroperoxide (LH) content was also unchanged in C57BL/6J mice dosed acutely with ADR. However, hepatic LH content increased rapidly following treatment with ADR, reaching maximal level 1 day following treatment before returning to below untreated levels 24 hours later. Studies with genetically acatalasemic C57BL/6J mice showed that neither cardiac nor hepatic lipid hydroperoxide content in ADR-dosed animals is affected by tissue catalase levels. These results demonstrate that C57BL/6J mouse heart is refractory to ADR-induced lipid peroxidation (LP) although overall mortality from the drug is unaffected, and do not support the hypothesis that ADR-induced mortality in mice is a consequence of cardiac LP.