Inhibition of enzyme acetylcholinesterase (AChE, EC 3.1.1.7.) at central nervous system by highly toxic organophosphorus compounds (OPC) causes a cholinergic crisis which is the most probable “trigger” mechanism for the convulsive activity observed after intoxication. It is known that the convulsions produced by OPC may cause brain damages and long-term effects with neurobehavioral, cognitive and neuromuscular disturbances (McLeod, 1985; USAMRICD report, 1998). Therefore the abolishment of convulsions plays a very important role in the prophylactic of organophosphorus poisoning. Significant attention has been paid to this problem during last years but it is yet not resolved. There are different pharmacological approaches to prevent or abolish the convulsive activity. The pretreatment with a potent central acting cholinolytic combined with a cholinesterase reactivator may ameliorate to a great extent the symptoms of OP intoxication and to prevent the delayed neuropathy as well. In previous investigations a relatively high anticonvulsive activity of biperiden have been demonstrated (Anderson et al., Capacio, Shih, 1991)....

Keywords: HI-6; acetylcholinesterase; toxicology