Siegers C P, Younes M
Arzneimittelforschung. 1979;29(3):520-3.
2-Dimethylaminoethanol (DMAE; 0.1--0.5 g/kg) significantly reduced the paracetamol-induced increments of serum-enzyme activities (GOT, GPT, SDH) in rats and mice. This hepatoprotective effect of DMAE depended on the applied dose in rats, but there was no complete protection following the highest dose. Paracetamol-induced depletion of hepatic glutathione (GSH) was not influenced by the simultaneous administration of DMAE in rats and mice. Metabolic disposition of paracetamol in the urine of rats showed an enhanced elimination of free paracetamol and the glucuronide in the DMAE-treated group, whereas the mercapturate excretion remained unchanged. Diminished p-hydroxylation of aniline in a 9000Xg supernatant of rat and mouse liver homogenates in the presence of DMAE indicated an inhibition of microsomal mixed-function oxidase activity, which is also involved in the metabolic activation of paracetamol.
2-二甲基氨基乙醇（DMAE；0.1--0.5克/千克）显著降低了扑热息痛诱导的大鼠和小鼠血清酶活性（谷草转氨酶、谷丙转氨酶、山梨醇脱氢酶）的升高。DMAE的这种肝脏保护作用在大鼠中取决于给药剂量，但在最高剂量后没有完全保护作用。扑热息痛诱导的肝脏谷胱甘肽（GSH）耗竭不受大鼠和小鼠同时给予DMAE的影响。大鼠尿液中扑热息痛的代谢处置表明，在DMAE处理组中，游离扑热息痛和葡萄糖醛酸苷的消除增加，而硫醚氨酸排泄保持不变。在存在DMAE的情况下，大鼠和小鼠肝脏匀浆9000Xg上清液中苯胺的对羟基化减少，表明微粒体混合功能氧化酶活性受到抑制，该酶也参与扑热息痛的代谢活化。
