Acute adriamycin cardiotoxicity in rats.

To explore the possible occurrence and pathogenic implications of in vivo heart lipoperoxidation in the acute model of ADR-cardiotoxicity, male Wistar rats were injected i.v. with a single dose of ADR (15 mg/kg) and the controls with saline. The rats were killed at 24 and 96 hr after treatment and at the later period the serum levels of creatine kinase of ADR-treated rats were significantly elevated. ADR-treatment did not significantly modify the cardiac concentrations of DNA, RNA, protein, the levels of activity of cardiac catalase and GSH-Px or the in vitro production of malonaldehyde of cardiac homogenates. Mitochondrial swelling at 24 hr and reduction of the mitochondrial numerical and volumetric densities along with myofilament fragmentation at 96 hr were the most significant ultrastructural changes in cardiac myocytes of ADR-treated rats. Although in vivo lipoperoxidation (diene conjugation) was detected in the cardiac lipids of only 2 out of 6 rats at 24 hr and in 3 out of 6 rats at 96 hr, no clear correlation could be found between the eventual presence of this in vivo phenomenon and any of the cardiac changes. These data suggested that lipoperoxidation may not play a fundamental role in the pathogenesis of acute ADR-cardiotoxicity in rats.