Ham E A, Egan R W, Soderman D D, Gale P H, Kuehl F A
J Biol Chem. 1979 Apr 10;254(7):2191-4.
A study of the enzymes of the arachidonic acid cascade revealed a high sensitivity of prostacyclin synthetase and a complete resistance of thromboxane A2 synthetase to time-dependent destruction by an oxidant [Ox] released during the peroxidase-catalyzed reduction of hydroperoxy fatty acids. The destructive action of [Ox] derived from prostaglandin G1 (PGG1), 15-hydroperoxy-PGE1, 15-hydroperoxy-5,8,11,13-eicosatetraenoic acid, and 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid upon prostacyclin synthetase was prevented by 2-aminomethyl-4-t-butyl-6-iodophenol. On the other hand, deactivation resulting from PGG2 metabolism was neither time-dependent nor sensitive to 2-aminomethyl-4-t-butyl-6-iodophenol. The possibility that the action of [Ox] may alter the arachidonic acid cascade in favor of thromboxane A2 is discussed in view of its possible implications in inflammatory and other pathological processes.
一项关于花生四烯酸级联反应中各种酶的研究表明,前列环素合成酶对氧化剂[Ox]导致的时间依赖性破坏高度敏感,而血栓素A2合成酶则完全抵抗这种破坏。这里的[Ox]是在过氧化物酶催化的氢过氧脂肪酸还原过程中释放出来的。源自前列腺素G1(PGG1)、15-氢过氧-PGE1、15-氢过氧-5,8,11,13-二十碳四烯酸和12-氢过氧-5,8,10,14-二十碳四烯酸的[Ox]对前列环素合成酶的破坏作用可被2-氨基甲基-4-叔丁基-6-碘苯酚阻止。另一方面,由PGG2代谢导致的失活既不依赖时间,也对2-氨基甲基-4-叔丁基-6-碘苯酚不敏感。鉴于[Ox]的作用可能在炎症及其他病理过程中有潜在影响,本文讨论了其可能改变花生四烯酸级联反应并有利于血栓素A2生成的可能性。