Appel K E, Rickart R, Schwarz M, Kunz H W
Arch Toxicol Suppl. 1979(2):471-7. doi: 10.1007/978-3-642-67265-1_59.
The alkylation of liver macromolecules following in vivo administration of dimethylnitrosamine (DMN) was diminished after phenobarbital or 3-methylcholanthrene induction of the microsomal monooxygenase system, but increased after SKF 525 A pretreatment. Determination of CH2O and CH3+formation in microsomal incubation systems revealed the same results for low DMN concentrations. An interpretation is given on the basis of spectrophotometric data and electron spinresonance (EPR) measurements, by proposing that metabolic inactivation of nitrosamines is catalysed by a reduction process in which cyt. P 450 seems to be involved.
体内给予二甲基亚硝胺（DMN）后，肝大分子的烷基化在苯巴比妥或3 - 甲基胆蒽诱导微粒体单加氧酶系统后减少，但在SKF 525 A预处理后增加。微粒体孵育系统中CH2O和CH3+形成的测定对于低DMN浓度显示出相同的结果。根据分光光度数据和电子自旋共振（EPR）测量结果给出了解释，提出亚硝胺的代谢失活是由一个还原过程催化的，其中细胞色素P 450似乎参与其中。
