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Cardiac oxygen radical metabolism in adriamycin induced cardiotoxicity


, : Cardiac oxygen radical metabolism in adriamycin induced cardiotoxicity. Jikeikai Medical Journal 37(2): 253-264

Adriamycin-induced free radicals have been suggested as one of the mechanisms for its cardiotoxic action. The aim of this study is to investigate the involvement of free radicals, free radical scavengers, and glutathione system in adriamycin cardiotoxicity. Adriamycin (ADR: 1 mg/kg/day) was administered intraperitoneally to rats for 3 weeks (total dose, 15 mg.kg). Myocardial lipid peroxide of the ADR group was increased as compared to the control group (control vs. ADR: 0.73 .+-. 0.14 vs. 1.16 .+-. 0.07 mDA/mg). The increase of myocardial lipid peroxide of ADR group was accompanied by the increase of glutathione peroxidase (control vs. ADR: 0.59 .+-. 0.07 vs. 0.75 .+-. 0.08.mu.M Nicotinamide adenine dinucleotide phosphate reduced form (NADPH) oxidized/min/mg), glutathione reductase (control vs. ADR: 51.2 .+-. 8.4 vs. 60.5 .+-. 4.2 Ut/mg), and catalase (control vs. ADR: 2.37 .+-. 0.83 vs. 3.31 .+-. 0.56 Ut/mg) in heart tissues. However, superoxide dismutase and glutathione content (oxidized and reduced form) in heart tissues were not altered. These results suggest that myocardial lipid peroxidation enhanced by ADR deteriorates myocardial membrane integrity in spite of endogenous defensive mechanisms in heart tissues.

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