Hartley A, Rice-Evans C
Department of Neurological Science, Royal Free Hospital School of Medicine, London, United Kingdom.
Arch Biochem Biophys. 1992 Sep;297(2):377-82. doi: 10.1016/0003-9861(92)90687-r.
Nonheme, nonferritin iron has been detected in membrane preparations from sickle erythrocytes and has been suggested to catalyze free radical reactions in these cells contributing to the development of membrane oxidation. In this study the hydroxypyridinone iron chelator, CP094, currently being evaluated as a potentially therapeutic chelator, and desferrioxamine have been studied for their abilities to chelate the nonheme iron within intact sickle erythrocytes under physiological conditions. The results suggest that CP094 can enter sickle erythrocytes, chelate nonheme iron and suppress membrane lipid peroxidation within a timescale in which desferrioxamine does not enter the cells. Suppression of lipid peroxidation showed no protective effect in an in vitro system inducing the formation of irreversibly sickled cells.
在镰状红细胞的膜制剂中已检测到非血红素、非铁蛋白铁，有人认为它可催化这些细胞中的自由基反应，从而导致膜氧化。在本研究中，羟基吡啶酮铁螯合剂CP094（目前正在作为一种潜在的治疗性螯合剂进行评估）和去铁胺对其在生理条件下螯合完整镰状红细胞内非血红素铁的能力进行了研究。结果表明，CP094可以进入镰状红细胞，螯合非血红素铁，并在去铁胺未进入细胞的时间范围内抑制膜脂质过氧化。在诱导不可逆镰状细胞形成的体外系统中，脂质过氧化的抑制没有显示出保护作用。
