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In order to elucidate the biochemical mechanism by which doxorubicin (DX) induces cumulative dose-dependent cardiomyopathy, the effect of DX on beating and on lipid peroxide level in myocardial cells was investigated by using a mouse myocardial cell culture system. Inhibition by DX of the beating of cultured myocardial cells was dose-and exposure time-dependent. When incubated with DX for 0.5 h, the number of beating cells decreased to 74% at 172 μM, 52% at 345 μM and 37% at 517 μM, and the lipid peroxide level in the cells increased significantly at 345 μM DX or more. At the low dose of 3.5 μM DX, though the number of beating cells decreased to 72% at 24 h, the lipid peroxide level in the cells was about the same as that without DX at 24 h, and increased to about 1.5 times that of the control at 48 h. Under the same conditions as above, 120μM α-tocopherol (Toc) added in advance of the treatment reduced by 86% the lipid peroxidation by DX, but did not protect the beating from DX toxicity. In contrast, 120 μM coenzyme Q10 (CoQ10) reduced the lipid peroxidation by only 33%, but increased the number of beating cells at 48 h from 42% to 68%. We conclude that the lipid peroxidation by DX does not initiate the beat inhibition of cultured myocardial cells, and that the protective effect of CoQ10 on beating is also based on biochemical actions other than reduction of the lipid peroxidation.

Evidence that lipid peroxidation by doxorubicin does not initiate the beat inhibition of cultured mouse myocardial cells.