Maridonneau I, Garay R P, Braquet P
Biomed Biochim Acta. 1983;42(11-12):S58-62.
We have reported that the generation of oxygen free radicals within human red cells resulting from treatment with phenazine methosulfate (PMS) induces several toxic effects in membranes; lipid peroxidation, a binding of methemoglobin and a loss of intracellular K+. The specific K+ carriers are only slightly inhibited (Na+, K+ pump; Na+, K+ cotransport) and the K+ loss is mainly due to an increase in the passive K+ permeability. This could result from a toxic effect on the membrane such as lipid peroxidation or methemoglobin binding. The use of "oxygen free radical scavenger" molecules and pro-oxidative molecules showed that the PMS-dependent increase in passive K+ permeability is consequent to lipid peroxidation rather than to methemoglobin binding.
我们曾报道,用硫酸甲酯吩嗪(PMS)处理人红细胞会导致细胞内产生氧自由基,进而在细胞膜上引发多种毒性效应,包括脂质过氧化、高铁血红蛋白结合以及细胞内钾离子流失。特定的钾离子载体仅受到轻微抑制(钠钾泵;钠钾协同转运),钾离子流失主要是由于被动钾离子通透性增加所致。这可能是对细胞膜的毒性作用,如脂质过氧化或高铁血红蛋白结合所导致的。使用“氧自由基清除剂”分子和促氧化分子的实验表明,PMS 依赖的被动钾离子通透性增加是脂质过氧化的结果,而非高铁血红蛋白结合的结果。