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Addition of 0.5mm-daunomycin, a quinone anti-cancer drug, causes severe inhibition of respiration in Ehrlich ascites cells, whereas Yoshida ascites cells were almost as resistant as rat hepatocytes. An inverse relationship appears to exist in the two types of tumour cells (which are both catalase-deficient) between the extent of cellular damage brought about by intracellular formation of superoxide anion occurring on reaction with O(2) of the drug free radical and the efficiency of the glutathione-mediated H(2)O(2)-detoxifying system.

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