Messiha F S
Vet Hum Toxicol. 1984;26 Suppl 2:38-40.
The effect of short-term intake of LiCl in drinking water on mouse liver alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenase (L-ALDH) was studied in the albino and in the C57BL mouse strain. The Li-treatment induced initially mitochondrial L-ALDH which was followed by L-ADH in the albino mouse. This was not apparent in the C57 mouse strain. There was an induction of hepatic L-ADH and L-ALDH in the C57BL mouse subsequent to short-term administration of chlorpromazine (CPZ). Coadministration of LiCl with CPZ resulted in moderate enhancement of enzymatic activity per mg wet liver tissue from corresponding controls. Chlorpromazine inhibited rat liver and testicular ADH when tested in vitro. Both cytoplasmic and mitochondrial ALDH were not altered by CPZ in vitro. The results suggest that alcohol consumption during treatment with both drugs studied could evoke metabolic adverse reactions which appear to be both species and strain dependent.
研究了在饮用水中短期摄入氯化锂对白化小鼠和C57BL小鼠品系肝脏乙醇脱氢酶(L-ADH)和乙醛脱氢酶(L-ALDH)的影响。在白化小鼠中,锂处理最初诱导了线粒体L-ALDH,随后是L-ADH。这在C57小鼠品系中并不明显。在短期给予氯丙嗪(CPZ)后,C57BL小鼠的肝脏L-ADH和L-ALDH有诱导作用。氯化锂与氯丙嗪共同给药导致每毫克湿肝组织的酶活性相对于相应对照组有适度增强。在体外试验中,氯丙嗪抑制大鼠肝脏和睾丸的ADH。体外实验中,CPZ对细胞质和线粒体ALDH均无影响。结果表明,在使用这两种研究药物治疗期间饮酒可能会引发代谢不良反应,这似乎与物种和品系有关。