Karpilovskaia E D, Rubenchik B L
Biull Eksp Biol Med. 1977 Dec;84(12):717-9.
Oral administration of dimethylamine, sodium nitrite and a combination of these precursors of endogenously synthesized dimethylnitrosamine to rats increased the activity of demethylase of this carcinogen in the liver microsomes. Under conditions of chronic experiment inclusion of dimethylamine into the diet of rats intensified the demethylase activity even in the presence of casein, an inductor of this enzymatic system. An inhibitor of protein synthesis--actinomycin D prevented an increase of demethylase activity in the microsomal fraction caused by dimethylamine.
给大鼠口服二甲胺、亚硝酸钠以及这些内源性合成二甲基亚硝胺前体的组合，会增加肝脏微粒体中这种致癌物的脱甲基酶活性。在慢性实验条件下，将二甲胺添加到大鼠饮食中，即使存在该酶系统的诱导剂酪蛋白，也会增强脱甲基酶活性。蛋白质合成抑制剂放线菌素D可阻止由二甲胺引起的微粒体部分脱甲基酶活性增加。
