Differential cytotoxicity of daunomycin in tumour cells is related to glutathione-dependent hydrogen peroxide metabolism

Abstract
Addition of 0.5 mM-daunomycin, a quinone anticancer drug, causes severe inhibition of respiration in [mouse] Ehrlich ascites carcinoma cells; [rat] Yoshida ascites Sarcoma cells were almost as resistant as rat hepatocytes. An inverse relationship appears to exist in the 2 types of tumor cells (which are both catalase-deficient) between the extent of cellular damage brought about by intracellular formation of superoxide anion occurring on reaction with O2 of the drug free radical and the efficiency of the glutathione-mediated H2O2-detoxifying system.