Baker M T, Van Dyke R A
Biochem Pharmacol. 1984 Jan 15;33(2):255-60. doi: 10.1016/0006-2952(84)90483-0.
Dichlorodi[U-14C]phenyltrichloroethane ( [14C]DDT), incubated with rat hepatic microsomes and NADPH, produced reactive intermediates which covalently bound to microsomal protein and lipids. In atmospheric oxygen, DDT bound to microsomal protein; however, binding was increased up to approximately 70% by oxygen depletion. Low levels of [14C]DDT binding to microsomal lipids occurred under atmospheric oxygen but, in contrast to protein binding, DDT-phospholipid binding was increased up to 20-fold by oxygen depletion. Dichlorodiphenyldichloroethane (DDD) was rapidly formed from DDT under anaerobic conditions, although when DDD was utilized as substrate, binding to microsomal protein occurred only in the presence of oxygen. Sodium dithionite, added to microsomes, produced [14C]DDT phospholipid and protein binding, and DDD formation, but failed to support DDD metabolism or binding. The data are consistent with the reductive formation of a DDT free-radical intermediate that led to the formation of DDD and that was bound preferentially to microsomal lipids.
二氯二[U-¹⁴C]苯基三氯乙烷（[¹⁴C]滴滴涕）与大鼠肝微粒体及还原型辅酶Ⅱ一起温育时，会产生与微粒体蛋白和脂质共价结合的反应性中间体。在大气氧环境中，滴滴涕会与微粒体蛋白结合；然而，通过耗尽氧气，结合量可增加约70%。在大气氧环境下，有少量的[¹⁴C]滴滴涕与微粒体脂质结合，但与蛋白结合不同的是，通过耗尽氧气，滴滴涕-磷脂结合量可增加20倍。在厌氧条件下，滴滴涕可迅速形成二氯二苯二氯乙烷（DDD），不过当DDD用作底物时，只有在有氧存在的情况下才会与微粒体蛋白结合。向微粒体中加入连二亚硫酸钠，会产生[¹⁴C]滴滴涕与磷脂和蛋白的结合以及DDD的形成，但无法支持DDD的代谢或结合。这些数据与滴滴涕自由基中间体的还原形成一致，该中间体导致了DDD的形成，并优先与微粒体脂质结合。
