Zanoli P
Arzneimittelforschung. 1979;29(12):1885-8.
2,4-Monofurfurylidene-tetra-O-methyl sorbitol (MSF), which prevents hepatotoxic effects of amanita phalloides powder (APP) in mice and of CCl4 in rats, increases liver microsomal drug-metabolizing activity in mice, as shown by a) the prolongation of pentobarbital or zoxazolamine-induced loss of the righting reflex and b) the decrease of phenylbutazone plasma levels. Further phenobarbital sodium, administered according the schedule usual for liver microsomal drug-metabolizing enzyme induction, also protects mice from APP death. On the other hand 2-diethylamino-ethyl-2,2-diphenylvalerate HCl (SKF 525-A) aggravates APP-toxicity and reduces APP protection afforded by both MSF and phenobarbital. Since it has been widely recognized that liver microsomal drug-metabolizing enzymes toxify phalloidin as well as CCl4, it is suggested that 1. mice APP toxicity depends on an unknown factor similar to but not identical to phalloidin, 2. MSF-antitoxic effect is produced by a mechanism unrelated to stimulation of liver microsomal drug-metabolizing system.
2,4-单糠叉基-四-O-甲基山梨醇（MSF）可预防小鼠中鹅膏蕈毒粉（APP）以及大鼠中四氯化碳的肝毒性作用，还可增强小鼠肝脏微粒体的药物代谢活性，这表现为：a）戊巴比妥或唑沙宗诱导的翻正反射消失时间延长；b）苯丁唑酮血浆水平降低。此外，按照常用于诱导肝脏微粒体药物代谢酶的方案给予苯巴比妥钠，也可保护小鼠免于APP致死。另一方面，盐酸2-二乙氨基乙基-2,2-二苯基戊酸酯（SKF 525-A）会加重APP毒性，并降低MSF和苯巴比妥所提供的APP保护作用。由于人们已广泛认识到肝脏微粒体药物代谢酶会使鬼笔环肽以及四氯化碳产生毒性，因此有人提出：1. 小鼠的APP毒性取决于一种与鬼笔环肽相似但不完全相同的未知因素；2. MSF的抗毒作用是通过一种与刺激肝脏微粒体药物代谢系统无关的机制产生的。
