Clark I A, Cowden W B, Hunt N H, Maxwell L E, Mackie E J
Br J Haematol. 1984 Jul;57(3):479-87. doi: 10.1111/j.1365-2141.1984.tb02922.x.
Intravenous injection of divicine into mice infected with Plasmodium vinckei rapidly killed the parasites and caused haemolysis. Degenerating parasites were observed frequently inside intact circulating erythrocytes, implying that parasite death was not a passive consequence of haemolysis. Both parasite death and haemolysis were prevented by the iron chelator desferrioxamine. In vitro, divicine caused the accumulation of malonyldialdehyde and the depletion of reduced glutathione in normal mouse erythrocytes. Desferrioxamine inhibited the former event, but not the latter. These observations support the hypothesis advanced by Huheey & Martin (Experientia, 31, 1145, 1975) to explain the patchy geographical distribution of glucose-6-phosphate dehydrogenase deficiency in historic malarial areas and also suggest that desferrioxamine, a drug already in clinical use, is a potential treatment for favism and other examples of oxidative haemolysis.
给感染文氏疟原虫的小鼠静脉注射蚕豆嘧啶，可迅速杀死疟原虫并导致溶血。在完整的循环红细胞内经常观察到退化的疟原虫，这意味着疟原虫的死亡并非溶血的被动结果。铁螯合剂去铁胺可预防疟原虫死亡和溶血。在体外，蚕豆嘧啶可导致正常小鼠红细胞中丙二醛的积累和还原型谷胱甘肽的消耗。去铁胺抑制了前者，但未抑制后者。这些观察结果支持了胡希和马丁（《实验》，31，1145，1975）提出的假设，以解释历史上疟疾流行地区葡萄糖-6-磷酸脱氢酶缺乏症的片状地理分布，同时也表明，已在临床使用的药物去铁胺是治疗蚕豆病和其他氧化性溶血病例的潜在药物。
