al-Harbi M M, al-Gharably N M, al-Shabanah O A, al-Bekairi A M, Osman A M, Tawfik H N
Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Cancer Chemother Pharmacol. 1992;31(3):200-4. doi: 10.1007/BF00685548.
Biochemical and histopathological evaluations of the protective effects of the iron-chelator desferrioxamine against the cardiac and haematological toxicities of doxorubicin in normal rats were carried out. A single dose of doxorubicin (15 mg/kg, i.v.) caused myocardial damage that manifested biochemically as an elevation of serum cardiac enzyme [glutamic oxaloacetic transaminase (GOT), lactic dehydrogenase (LDH) and creatine phosphokinase (CPK)] and cardiac isoenzyme levels and histopathologically as a swelling and separation of cardiac muscle fibers. Doxorubicin caused severe leucopenia and decreases in red blood cell counts and haemoglobin concentrations at 72 h after its administration. Desferrioxamine treatment (250 mg/kg, i.p.) carried out 30 min before doxorubicin administration protected the heart and blood elements from the toxic effects of doxorubicin as indicated by the recovery of levels of cardiac enzymes and isoenzymes and of red blood cell counts to normal values and by the absence of significant myocardial lesions. The findings of this study suggest that desferrioxamine can potentially be used clinically to prevent doxorubicin-induced cardiac and haematological toxicities.
开展了铁螯合剂去铁胺对正常大鼠阿霉素心脏毒性和血液毒性保护作用的生化及组织病理学评估。单次静脉注射阿霉素（15 mg/kg）可导致心肌损伤，生化表现为血清心脏酶[谷草转氨酶（GOT）、乳酸脱氢酶（LDH）和肌酸磷酸激酶（CPK）]及心脏同工酶水平升高，组织病理学表现为心肌纤维肿胀和分离。阿霉素给药72小时后可导致严重白细胞减少以及红细胞计数和血红蛋白浓度降低。在阿霉素给药前30分钟进行去铁胺治疗（250 mg/kg，腹腔注射），可保护心脏和血液成分免受阿霉素的毒性影响，表现为心脏酶和同工酶水平以及红细胞计数恢复至正常水平，且无明显心肌病变。本研究结果表明，去铁胺可能在临床上用于预防阿霉素引起的心脏和血液毒性。
