Enhanced Neurotoxicity of 3,3'-Iminodipropionitrile Following Pretreatment withCarbon Tetrachloride in the Rat

摘要

The work tested the hypothesis that IDPN must be metabolized by the liver to anactive metabolite to become neurotoxic. Thus a reduction in IDPN neurotoxicity would be expected when liver function is compromised. Male Long-Evans rats were given ip injections of saline, 100 (IDPN1) or 200 (IDPN2) mg/kg of IDPN for three days. Half of the animals in each IDPN dose group received corn oil po and the other half 1 g/kg of the hepatotoxicant carbon tetrachloride (CCl4) for three days, starting one day before IDPN administration. Motor activity and acoustic startle response (ASR) were monitored prior to, and 1, 3, 9 and 16 weeks after IDPN exposure. An observational rating score was obtained at 1, 3 and 9 weeks.