Accumulation of malondialdehyde in mouse heart following acute dosing with adriamycin is strain specific and unaffected by cardiac catalase status.
CDF1 and C57BL/6J male mice were acutely dosed with Adriamycin (ADR), and total cardiac malondialdehyde (MDA) quantitated following isolation by modification of previously developed procedures. Cardiac MDA content in CDF1 mice increased significantly 5 days following ADR dosing as reported by others, but was unchanged in C57BL/6J mice. ADR-induced mortality and a significant loss in cardiac weight 2-3 days after treatment was similar in both strains. Cardiac lipid hydroperoxide (LH) content was also unchanged in C57BL/6J mice dosed acutely with ADR. However, hepatic LH content increased rapidly following treatment with ADR, reaching maximal level 1 day following treatment before returning to below untreated levels 24 hours later. Studies with genetically acatalasemic C57BL/6J mice showed that neither cardiac nor hepatic lipid hydroperoxide content in ADR-dosed animals is affected by tissue catalase levels. These results demonstrate that C57BL/6J mouse heart is refractory to ADR-induced lipid peroxidation (LP) although overall mortality from the drug is unaffected, and do not support the hypothesis that ADR-induced mortality in mice is a consequence of cardiac LP.
Baird
M B
MB
Masonic Medical Research Laboratory, Utica, New York 13501-1787.
Hough
J L
JL
Sfeir
G T
GT
D000818:Animals; D002374:Catalase / Q000502:physiology*; D004317:Doxorubicin / Q000008:administration & dosage / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D007274:Injections, Intraperitoneal; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D013045:Species Specificity
D008315:Malondialdehyde; D004317:Doxorubicin; D002374:Catalase