Hölzel C, Spiteller G
Lehrstuhl Organische Chemie 1 der Universität, Bayreuth.
Naturwissenschaften. 1995 Oct;82(10):452-60.
In diseases leading to massive acute cell damage, e.g., myocardial infarction or spontaneous inflammation, increased amounts of hydroperoxides of unsaturated fatty acids (LOOH) are found. An even higher production of LOOH is observed in homogenized tissue. If cells are injured, dormant lipoxygenases (LOX) are inevitably activated. They oxidize unsaturated membrane fatty acids to LOOH. This process involves not only arachidonic acid - as tacitly assumed up to now - but also linoleic acid. LOOH are decomposed to chemically highly reactive species, some of which were previously unknown (e.g, alpha-hydroxyaldehydes). LOO. radicals can also transform any molecule with a double bond to an epoxide. Therefore, epoxides are found in injured tissue. The same degradation products of hydroperoxides have been observed in elevated amounts in acute cell injury and in chronic diseases, e.g., atherosclerosis, psoriasis, and rheumatoid diseases. Therefore, we conclude that in these cases too, increased generation of hydroperoxides is caused by gradual cell injury liberating lipoxygenases.
在导致大量急性细胞损伤的疾病中，如心肌梗死或自发性炎症，会发现不饱和脂肪酸氢过氧化物（LOOH）的含量增加。在匀浆组织中观察到LOOH的产量甚至更高。如果细胞受损，休眠的脂氧合酶（LOX）不可避免地会被激活。它们将不饱和膜脂肪酸氧化为LOOH。这个过程不仅涉及花生四烯酸——如迄今为止默认的那样——还涉及亚油酸。LOOH分解为化学性质高度活泼的物质，其中一些以前未知（例如α-羟基醛）。LOO·自由基还可以将任何具有双键的分子转化为环氧化物。因此，在受损组织中会发现环氧化物。在急性细胞损伤和慢性疾病，如动脉粥样硬化、牛皮癣和类风湿性疾病中，也观察到氢过氧化物的相同降解产物含量升高。因此，我们得出结论，在这些情况下，氢过氧化物生成增加也是由逐渐的细胞损伤释放脂氧合酶所致。
