PMID: 6411900Sep 1, 1983Paper

Stimulation of mouse heart and liver microsomal lipid peroxidation by anthracycline anticancer drugs: characterization and effects of reactive oxygen scavengers

The Journal of Pharmacology and Experimental Therapeutics
E G MimnaughM A Trush

Abstract

The interaction of adriamycin or several other quinone-containing anthracycline anticancer drugs with mouse heart or liver microsomes resulted in greatly enhanced NADPH oxidation and 5- to 10-fold stimulation of NADPH-dependent, reactive oxygen-mediated microsomal lipid peroxidation. Adriamycin, daunorubicin, desacetyladriamycin and aclacinomycin A all stimulated lipid peroxidation maximally when included at concentrations of 100 to 200 microM, whereas carminomycin and 4-demethoxydaunorubicin produced equivalent enhancement of peroxidation at lower concentrations of 30 to 50 microM. Mitomycin C markedly increased heart microsomal lipid peroxidation, but, interestingly, had little effect when liver microsomes were used. In contrast, 5-imino-daunorubicin and alkylaminoanthracenedione inhibited both heart and liver microsomal lipid peroxidation. NADPH supported anthracycline-stimulated lipid peroxidation, however, an NADPH-generating system provided greater activity. NADH was only about 50% as effective as NADPH and served as cofactor with liver microsomes but not with heart microsomes. Scavengers of reactive oxygen such as superoxide dismutase, reduced glutathione and 1,3-dimethylurea diminished the anthracycline-stimulated heart...Continue Reading

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