Abstract
Ethane expiration, which indicates lipid peroxidation, was determined immediately, 1 day, and 2 days after i.p. injection of doxorubicin (20, 45, and 65 mg/kg) in rats in vivo. None of these doses caused a significant increase in ethane formation, except a small elevation on the 2nd day after 45/kg. Treatment with 65 mg/kg was lethal within 24 hours, although no increase in ethane production was measured during the first 6 hours after administration. These results suggest that acute lipid peroxidation may not occur during doxorubicin metabolism in the rat and may not be one of the primary reactions in doxorubicin cardiotoxicity. Thus, cardio-protection by α-tocopherol and other free radical scavengers may be due rather to the trap of free oxygen radicals than to the prevention of lipid peroxidation during doxorubicin metabolism.
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Scheulen, M.E., Muliawan, H., Kappus, H. (1982). The Role of Acute Lipid Peroxidation in Doxorubicin Cardiotoxicity. In: Muggia, F.M., Young, C.W., Carter, S.K. (eds) Anthracycline Antibiotics in Cancer Therapy. Developments in Oncology, vol 10. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-7630-6_14
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