Carlin G
J Free Radic Biol Med. 1985;1(4):255-61. doi: 10.1016/0748-5514(85)90129-1.
Human polymorphonuclear leucocytes were found to promote peroxidation linolenic acid micelles. The peroxidation was markedly enhanced by addition of ferric iron, either in the form of chloride, ADP-complex or EDTA to the phosphate-buffered reaction mixture. The leucocyte oxygen burst was induced by the addition of the lipid micelles, and no other stimulatory agent was therefore required. Pretreatment of the leucocytes with cytochalasin B did not inhibit t.e lipid peroxidation which indicates that phagocytosis was not part of the peroxidative mechanism. Lipid peroxidation was inhibited by alpha-tocopherol acetate, butylated hydroxytoluene, manganese ions and desferrioxamine but not by superoxide dismutase, catalase or the hydroxyl radical scavenger dimethylsulfoxide. Lipid peroxidation promoted by xanthine oxidase, was studied for comparison. This was inhibited by superoxide dismutase, indicating that xanthine oxidase, in contrast to leucocytes, promotes lipid peroxidation via a superoxide-dependent mechanism. Manganese ions and butylated hydroxytoluene, and to a lesser extent alpha-tocopherol, were also inhibitors. The leucocyte promoted lipid peroxidation is similar to the well-known peroxidation promoted by microsomal NADPH-cytochrome P450 reductase, which also is not induced by superoxide radicals. Peroxidation of lipids may be a mechanism whereby granulocytes express tissue damage in for example inflammation and ischaemia.
已发现人类多形核白细胞可促进亚麻酸胶束的过氧化反应。向磷酸盐缓冲反应混合物中添加铁离子（以氯化物、ADP复合物或EDTA的形式）可显著增强过氧化反应。脂质胶束的添加可诱导白细胞的氧爆发，因此不需要其他刺激剂。用细胞松弛素B预处理白细胞并不抑制脂质过氧化，这表明吞噬作用不是过氧化机制的一部分。脂质过氧化受到醋酸α-生育酚、丁基化羟基甲苯、锰离子和去铁胺的抑制，但不受超氧化物歧化酶、过氧化氢酶或羟基自由基清除剂二甲基亚砜的抑制。为作比较，研究了黄嘌呤氧化酶促进的脂质过氧化。它受到超氧化物歧化酶的抑制，这表明与白细胞不同，黄嘌呤氧化酶通过超氧化物依赖性机制促进脂质过氧化。锰离子和丁基化羟基甲苯，以及程度较轻的α-生育酚也是抑制剂。白细胞促进的脂质过氧化类似于微粒体NADPH-细胞色素P450还原酶促进的众所周知的过氧化反应，后者也不是由超氧自由基诱导的。脂质过氧化可能是粒细胞在例如炎症和缺血中表达组织损伤的一种机制。
