Key result
Vitamin E deficiency fails to worsen doxorubicin-induced acute myocardial dysfunction, questioning lipid peroxidation's role.
Why the study?
The role of oxidative membrane damage and lipid peroxidation in the pathogenesis of acute doxorubicin-induced cardiotoxicity was unclear.
Does doxorubicin-induced lipid peroxidation cause acute cardiotoxicity in rat isolated hearts?
Does doxorubicin-induced lipid peroxidation cause acute cardiotoxicity in rat isolated hearts?
Lipid peroxidative damage is likely not the decisive mechanism in the development of acute doxorubicin-induced cardiomyopathy in rats.
May warrant antioxidant monitoring with doxorubicin; in vitro data leaves open clinical translation.
Doxorubicin induces an acute cardiotoxicity that becomes manifest in isolated hearts as a deterioration in mechanical function. The oxidative component in this myocardial damage has been investigated. The effects of doxorubicin on the activity of superoxide dismutase and the capacity of the glutathione system, factors of the cellular protective mechanism against free radicals, were examined in rat isolated heart. Doxorubicin was found to reduce the capacity of the protective mechanisms. Whether oxidative membrane damage due to excessive free radical formation plays a role in the pathogenesis of the acute cardiotoxic action of doxorubicin was also examined. Its acute effect on myocardial contraction amplitude, frequency of beating, coronary flow and on the above mentioned biochemical parameters was compared in rat hearts sufficient or deficient in vitamin E. Peroxidation of lipids was measured as the formation of malondialdehyde, one of the final products of this process. Vitamin E deficiency neither aggravated the decrease in the capacity of the cellular protective factors nor worsened the reduction in myocardial function. Nor did induction of lipid peroxidation by doxorubicin occur in vitamin E-deficient hearts. It was concluded that lipid peroxidative damage most probably is not decisive in the development of the acute cardiomyopathy in rats.
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Julicher et al. (1986) studied Acute doxorubicin-induced cardiotoxicity. Doxorubicin vs. Vitamin E sufficient vs deficient hearts was evaluated on Myocardial contraction amplitude, frequency of beating, coronary flow, and lipid peroxidation (malondialdehyde formation). Doxorubicin-induced lipid peroxidative damage is likely not decisive in the development of acute cardiomyopathy, as vitamin E deficiency did not worsen myocardial function reduction.
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