りん酸ビス[(1-メチルエチル)フェニル]フェニル

The potential of isopropyl triphenyl phosphate to produce delayed neurotoxicity in hens was examined using several techniques. Isopropyl triphenyl phosphate contained O,O,O-triphenyl phosphate (24%), O-O-isopropylphenyl O,O-diphenyl phosphate (25%), O,O-diisopropyl-phenyl O-phenyl phosphate (20%), O-O, p-diisopropylphenyl O,O-diphenyl phosphate (18%) and O-p-isopropylphenyl O,O-diphenyl phosphate (6%). Hens treated twice, 3 wk apart, with doses of isopropyl triphenyl phosphate as high as 11.7 g/kg showed no clinical signs of delayed neurotoxicity and only mild signs of general toxicity. Furthermore, none showed even subtle neurohistologic changes suggestive of delayed neurotoxicity. Isopropyl triphenyl phosphate produced dose-dependent inhibition of hen plasma cholinesterase and brain neurotoxic esterase. The study was continued because neurotoxic esterase inhibition has been shown to be a reliable predictor of organophosphates that produce delayed neurotoxicity. Isopropyl triphenyl phosphate was administered prior to tri-o-tolyl phosphate challenge in order to determine if it altered development of tri-o-tolyl phosphate delayed neurotoxicity. Isopropyl triphenyl phosphate neither enhanced nor reduced the onset or severity of neurotoxicity produced by tri-o-tolyl phosphate. The time-course for brain and spinal cord neurotoxic esterase inhibition by isopropyl triphenyl phosphate and tri-o-tolyl phosphate were compared and found to be different. The maximum brain neurotoxic esterase inhibition produced by isopropyl triphenyl phosphate (dose up to 11.7 g/kg) was never complete (always less than 90%), and spinal cord neurotoxic esterase inhibition was significantly less than that produced in the brain. In contrast, brain and spinal cord inhibition produced by 500 mg/kg tri-o-tolyl phosphate were equal and greater than 90%. This testing regimen showed that isopropyl triphenyl phosphate produced an effect on neurotoxic esterase at the biochemical level without producing clinical or neurohistologic abnormalities in treated hens. Furthermore, this biochemical effect was qualitatively different than that produced by the delayed neurotoxicant tri-o-tolyl phosphate. /Isopropyl triphenyl phosphate/