急慢性铁负荷(iron loading IL)对机体的危害已受到普遍的关注,过量的铁通常在网状内皮系统的巨噬细胞和实体组织如肝脏中堆积,在特殊情况下大量的铁也可聚集到红系前体细胞和网织红细胞中.本文旨在从总体上探索铁在膜脂质过氧化中的作用以确定可以减轻铁毒性的一些因素;寻找铁毒性作用的最初部位;并对地贫病人红细胞在铁过量时膜损伤机理方面的研究结果进行讨论.铁与脂质过氧化过氧化物和过氧化氢经Haber-Weiss反应可以产生游离羟自由基及一些有害氧衍生物,铁在这一过程中起着关键作用.急慢性铁中毒(iron toxicity IT)的一个重要特征即是脂质过氧化增加,有证据表明慢性铁负荷过重(iron overloading, IOL)时地贫病人及IL模型动物的器官中,脂质过氧化的降解产物丙二醛(MDA)浓度增加,组织中共轭双烯降解产物浓度也增加,此外在体外人和体内鼠中进行肝微粒 Harmful effects of iron loading IL on the body have received widespread attention. Excess iron usually accumulates in macrophages of the reticuloendothelial system and in solid tissues such as the liver, and in special cases large amounts of iron may also accumulate To erythroid precursors and reticulocytes.This paper aims to explore in general the role of iron in membrane lipid peroxidation to identify factors that may reduce iron toxicity; to look for the initial site of iron toxicity; Discussion of the results of studies on the mechanism of membrane damage in patients with poor erythrocytes during iron overload.High iron and lipid peroxides and hydrogen peroxide by Haber-Weiss reaction can produce free hydroxyl radicals and some harmful oxygen derivatives, iron in the This process plays a key role.One of the key features of iron toxicity IT is increased lipid peroxidation, evidence of thalassemia and IL in patients with chronic iron overload (IOL) In model animals, the concentration of malondialdehyde (MDA), a degradation product of lipid peroxidation, increased and the concentration of conjugated diene degradation products in the tissue also increased. In addition, in vitro and in vivo mice, hepatic microparticles