Mechanism of protection with 2,4-monofurfurylidene-tetra-O-methyl sorbitol (MSF) against Amanita phalloides toxicity in mice.

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.