Stroo W E
Department of Pharmacology, University of South Alabama, Mobile 36688.
Res Commun Chem Pathol Pharmacol. 1988 Dec;62(3):435-46.
Furazolidone and doxorubicin induce dilative cardiomyopathies but are not structurally similar. In order to determine if these drugs might share a common mechanism of action, the free radical based chemistry of these drugs were compared. Furazolidone like doxorubicin stimulates lipid peroxidation in the presence of added iron. However, while furazolidone (50 microM) stimulated lipid peroxidation 2.4 fold, doxorubicin (50 microM) increased lipid peroxidation 10 fold in the presence of iron (50 microM). In contrast, furazolidone was more potent than doxorubicin at stimulating the oxidation of epinephrine and the reduction of cytochrome c when incubated with cardiac sarcosomes. These data demonstrate that while both drugs stimulate free radical chemistry, they differ in their propensity to stimulate iron-dependent (lipid peroxidation) versus iron-independent reactions. Thus differences in the expression of these drugs pathology may be due to differences in their redox chemistry.
呋喃唑酮和阿霉素可诱发扩张型心肌病，但它们在结构上并不相似。为了确定这些药物是否可能具有共同的作用机制，对这些药物基于自由基的化学性质进行了比较。与阿霉素一样，呋喃唑酮在添加铁的情况下会刺激脂质过氧化。然而，在存在50微摩尔铁的情况下，虽然50微摩尔的呋喃唑酮能使脂质过氧化增加2.4倍，但50微摩尔的阿霉素能使脂质过氧化增加10倍。相反，当与心肌肌质体一起孵育时，呋喃唑酮在刺激肾上腺素氧化和细胞色素c还原方面比阿霉素更有效。这些数据表明，虽然两种药物都能刺激自由基化学反应，但它们在刺激铁依赖性（脂质过氧化）与铁非依赖性反应的倾向方面存在差异。因此，这些药物病理表现的差异可能是由于它们氧化还原化学性质的不同。
