| First Author | Baird MB | Year | 1993 |
| Journal | Res Commun Chem Pathol Pharmacol | Volume | 80 |
| Issue | 3 | Pages | 363-6 |
| PubMed ID | 8351415 | Mgi Jnum | J:14496 |
| Mgi Id | MGI:62663 | Citation | Baird MB, et al. (1993) Accumulation of malondialdehyde in mouse heart following acute dosing with adriamycin is strain specific and unaffected by cardiac catalase status. Res Commun Chem Pathol Pharmacol 80(3):363-6 |
| abstractText | 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. |
