Delayed neuropathy and inhibition of soluble neuropathy target esterase following the administration of organophosphorus compounds to hens.
Delayed neuropathy and inhibition of soluble neuropathy target esterase (NTE) and acetylcholinesterase (AChE) activities in different regions of brain and spinal cord of adult hens were studied after the intravenous administration of leptophos (30 mg/kg), tri-o-cresyl phosphate (TOCP 40 mg/kg) or dipterex (200 mg/kg). The level of NTE activity varied according to the regions of the central nervous system (CNS) of the control (normal) hen, being higher in the cerebrum (74.1 micromol of phenyl valerate hydrolyzed/10 minutes/mg protein) and in the cerebellum (68.7), and lower in the spinal cord (44.5 in cervical, 55.6 in thoracic and 50.0 in lumbar cord). Hens given leptophos and TOCP demonstrated delayed neuropathy with obvious inhibition of NTE, but the times of onset and the degrees of peak inhibition of NTE activity were different: 6-24 hours after dosing and 73-82% of normal activity for leptophos, and 24-48 hours and 45-80% for TOCP, respectively. Furthermore, the average inhibition of NTE during 6-48 hours after dosing, (called here 'period average inhibition') was also significantly different between the leptophos group (63-73%) and TOCP group (40-64%). Hens given dipterex did not demonstrate delayed neuropathy, and had the least peak inhibition and period average inhibition of NTE activity among the 3 groups. Ratios of NTE inhibition/AChE inhibition were higher in the leptophos group (0.91-1.24) and TOCP group (1.13-2.45) than in the dipterex group (0.25-0.79). These results indicate that the distribution of NTE in the soluble fraction of membrane proteins is different in different regions of the CNS, and that the degree of peak inhibition of NTE activity and the time of onset of peak inhibition induced by organophosphorus compounds (OPs) also differ for different OPs. Thus, practical and useful NTE measurements should identify the peak inhibition and period inhibition in several nervous tissue regions.
Tian
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Y
Department of Public Health, School of Medicine, Mie University, Tsu, Japan. tianying@doc.medic.mie-u.ac.jp
Xie
X K
XK
Piao
F Y
FY
Yamauchi
T
T
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D002265:Carboxylic Ester Hydrolases / Q000037:antagonists & inhibitors*; D002645:Chickens; D005260:Female; D007275:Injections, Intravenous; D010773:Leptophos / Q000494:pharmacology; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000201:enzymology / Q000503:physiopathology; D009943:Organophosphorus Compounds / Q000494:pharmacology*; D012016:Reference Values; D012995:Solubility; D013997:Time Factors; D014236:Trichlorfon / Q000494:pharmacology; D014317:Tritolyl Phosphates / Q000494:pharmacology
D009943:Organophosphorus Compounds; D014317:Tritolyl Phosphates; D010773:Leptophos; D014236:Trichlorfon; D002265:Carboxylic Ester Hydrolases; C021859:neurotoxic esterase; D000110:Acetylcholinesterase; C025541:tri-o-cresyl phosphate