Messiha F S, Frost R E, Sproat H F
Drug Chem Toxicol. 1983;6(4):397-408. doi: 10.3109/01480548309082718.
Behavioral, biochemical and histological techniques were used to evaluate the possible interaction between a lithium salt and ethanol. Injection of a single dosage of ethanol into mice pretreated with LiCl for 14 days enhanced spontaneous locomotor activity for the initial 60 min of testing compared to respective control. Drinking of 0.4% of LiCl solution for 25 consecutive days induced hepatic alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenase (L-ALDH). The LiCl treatment increased Vmax of both enzymes in the same order and magnitude. The apparent Km of L-ADH was increased by LiCl while that of L-ALDH remained unchanged from respective controls. Organ histopathology indicates decreased germinal activity of the mouse spleen by the LiCl treatment. A mild chronic perivascular inflammation and slight hypercellularity of the myocardium was also noted in the heart of LiCl-treated mice.
采用行为学、生物化学和组织学技术来评估锂盐与乙醇之间可能的相互作用。与各自的对照组相比,向预先用LiCl处理14天的小鼠注射单剂量乙醇后,在最初60分钟的测试中增强了自发运动活性。连续25天饮用0.4%的LiCl溶液可诱导肝乙醇脱氢酶(L-ADH)和醛脱氢酶(L-ALDH)。LiCl处理以相同的顺序和幅度增加了两种酶的Vmax。LiCl使L-ADH的表观Km增加,而L-ALDH的表观Km与各自的对照组相比保持不变。器官组织病理学表明,LiCl处理可降低小鼠脾脏的生发活性。在LiCl处理的小鼠心脏中还观察到轻度慢性血管周围炎症和心肌轻度细胞增多。