This study aimed to evaluate the antidotal potency of
tenocyclidine (TCP) that probably might protect
acetylcholinesterase (AChE) in the case of
organophosphate poisoning. TCP was tested alone as a pretreatment or in combination with
atropine as a
therapy in rats poisoned with (1/4) and (1/2) of LD(50) of
soman. Possible genotoxic effects of TCP in white blood cells and brain tissue were also studied. Results were compared with previous findings on the adamantyl
tenocyclidine derivative
TAMORF. TCP given alone as pretreatment, 5 min before
soman, seems to be superior in the protection of
cholinesterase (ChE) catalytic activity in the plasma than in brain, especially after administration of the lower dose of
soman. Plasma activities of the
enzyme after a joint treatment with TCP and
soman were significantly increased at 30 min (P<0.001) and 24 h (P=0.0043), as compared to
soman alone. TCP and
atropine, given as
therapy, were more effective than TCP administered alone as a pretreatment. The above
therapy significantly increased activities of the
enzyme at 30 min (P=0.046) and 24 h (P<0.001), as compared to controls treated with (1/4) LD(50) of
soman alone. Using the alkaline comet assay, acceptable genotoxicity of TCP was observed. However, the controversial role of TCP in brain protection of
soman-poisoned rats should be studied further.