Golly I, Hlavica P, Wolf J
Biochem J. 1984 Dec 1;224(2):415-21. doi: 10.1042/bj2240415.
Irradiation with u.v. light of aerobic aqueous media containing both rabbit liver microsomal fraction and 4-chloroaniline results in N-oxidation of the arylamine. The reaction is severely blocked by exhaustive extraction with organic solvents of the microsomal membranes to remove lipids. Further, scavengers of OH. and O2.-impair the photochemical process. These findings suggest that the observed phenomenon may be closely associated with light-induced lipid peroxidation. Indeed, N-oxidation of 4-chloroaniline is fully preserved when either phospholipid liposomes or dispersed linoleic acid substitute for intact microsomal fraction. Co-oxidation of the amine substrate occurs during iron/ascorbate-promoted lipid peroxidation also, but H2O2 or free OH. radicals do not appear to be involved. Cumene hydroperoxide-sustained rabbit liver microsomal turnover of the amine generates N-oxy product via O2-dependent and -independent pathways; propagation of lipid peroxidation is presumed to govern the former route. Lipid hydroperoxides, either exogenously added to rabbit liver microsomal suspensions or enzymically formed from arachidonic acid in ram seminal-vesicle microsomal preparations, support N-oxidation of 4-chloroaniline. The significance, in arylamine activation, of lipid peroxidation in certain extrahepatic tissues exhibiting but low mono-oxygenase activity is discussed.
用紫外线照射含有兔肝微粒体部分和4-氯苯胺的需氧水性介质会导致芳胺的N-氧化。用有机溶剂彻底萃取微粒体膜以去除脂质会严重阻碍该反应。此外，OH·和O2-的清除剂会损害光化学过程。这些发现表明，观察到的现象可能与光诱导的脂质过氧化密切相关。事实上，当磷脂脂质体或分散的亚油酸替代完整的微粒体部分时，4-氯苯胺的N-氧化完全得以保留。在铁/抗坏血酸促进的脂质过氧化过程中也会发生胺底物的共氧化，但似乎不涉及H2O2或游离OH·自由基。异丙苯过氧化氢维持的兔肝微粒体对胺的转化通过O2依赖和非依赖途径生成N-氧产物；脂质过氧化的传播被认为控制着前一种途径。外源添加到兔肝微粒体悬浮液中的脂质氢过氧化物或在公羊精囊微粒体制剂中由花生四烯酸酶促形成的脂质氢过氧化物都支持4-氯苯胺的N-氧化。本文讨论了脂质过氧化在某些单加氧酶活性较低的肝外组织中芳胺活化中的意义。
