Minotti G, Aust S D
Institute of General Pathology, Catholic University, Rome, Italy.
Chem Biol Interact. 1989;71(1):1-19. doi: 10.1016/0009-2797(89)90087-2.
The role of iron in the peroxidation of polyunsaturated fatty acids is reviewed, especially with respect to the involvement of oxygen radicals. The hydroxyl radical can be generated by a superoxide-driven Haber-Weiss reaction or by Fenton's reaction; and the hydroxyl radical can initiate lipid peroxidation. However, lipid peroxidation is frequently insensitive to hydroxyl radical scavengers or superoxide dismutase. We propose that the hydroxyl radical may not be involved in the peroxidation of membrane lipids, but instead lipid peroxidation requires both Fe2+ and Fe3+. The inability of superoxide dismutase to affect lipid peroxidation can be explained by the fact that the direct reduction of iron can occur, exemplified by rat liver microsomal NADPH-dependent lipid peroxidation. Catalase can be stimulatory, inhibitory or without affect because H2O2 may oxidize some Fe2+ to form the required Fe3+, or, alternatively, excess H2O2 may inhibit by excessive oxidation of the Fe2+. In an analogous manner reductants can form the initiating complex by reduction of Fe3+, but complete reduction would inhibit lipid peroxidation. All of these redox reactions would be influenced by iron chelation.
本文综述了铁在多不饱和脂肪酸过氧化反应中的作用，尤其涉及氧自由基的参与情况。羟基自由基可通过超氧化物驱动的哈伯-维伊斯反应或芬顿反应产生；且羟基自由基可引发脂质过氧化。然而，脂质过氧化通常对羟基自由基清除剂或超氧化物歧化酶不敏感。我们提出羟基自由基可能不参与膜脂质的过氧化反应，相反，脂质过氧化需要Fe2+和Fe3+两者。超氧化物歧化酶无法影响脂质过氧化这一现象可通过铁能直接被还原这一事实来解释，以大鼠肝微粒体中依赖NADPH的脂质过氧化为例。过氧化氢酶可能具有促进、抑制或无影响的作用，因为过氧化氢可能将一些Fe2+氧化以形成所需的Fe3+，或者，过量的过氧化氢可能因Fe2+的过度氧化而产生抑制作用。以类似的方式，还原剂可通过还原Fe3+形成引发复合物，但完全还原会抑制脂质过氧化。所有这些氧化还原反应都会受到铁螯合作用的影响。
