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1 4 bis 2 2 hydroxyethylaminoethylamino 9 10 anthracenedione an anthra quinone anti tumor agent that does not cause lipid per oxidation in vivo comparison with daunorubicin


, : 1 4 bis 2 2 hydroxyethylaminoethylamino 9 10 anthracenedione an anthra quinone anti tumor agent that does not cause lipid per oxidation in vivo comparison with daunorubicin. Biochemical and Biophysical Research Communications 110(2): 399-405

Daunorubicin administration to mice produces a marked stimulation of lipid peroxidation in both liver and heart 48 h following administration. In direct contrast 1,4-bis{2-[(2-hydroxyethyl)amino]ethylamino}-9,10-anthracenedione (HAQ) does not induce lipid peroxidation in the liver and actually inhibits this event in the heart. In addition, neither daunorubicin nor HAQ deplete reduced glutathione [GSH] in liver or heart 48 h after drug administration. Daunorubicin induced GSH depletion was observed 2.5 h following administration. These results correlate with daunorubicin increased microsomal O2 consumption while HAQ produced no measurable effect on the rate of microsomal oxygen utilization. Apparently redox cycling to produce free radical O2 involved in lipid peroxidation and GSH depletion, an established action of daunorubicin, does not occur with HAQ. This apparent lack of HAQ reactivity may help explain the relatively low cardiotoxicity of this novel antitumor agent.

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