Diethylphosphorylation of rat cardiac M2 muscarinic receptor by chlorpyrifos oxon in vitro

Toxicol Lett. 2001 Feb 3;119(1):21-6. doi: 10.1016/s0378-4274(00)00294-0.

Abstract

The acute toxicity of chlorpyrifos oxon (CPO), the metabolically-activated form of the major organophosphorus insecticide chlorpyrifos, is attributable to diethylphosphorylation of acetylcholinesterase at its esteratic site. As a secondary effect, CPO is known to compete with agonist binding to the M2 muscarinic acetylcholine receptor (mAChR). This study tests the hypothesis that [ethyl-1,2-(3)H]CPO labels the M2 mAChR in rat cardiac membrane proteins. Of four labeled protein regions observed, only one had an apparent molecular mass (70-75 kDa) consistent with that of glycosylated M2 mAChR. It was identified as M2 muscarinic receptor by Western blotting and immunoprecipitation using a cardiac-specific M2 mAChR monoclonal antibody, providing the first direct evidence for diethylphosphorylation of a muscarinic receptor. This may be a functionally important M2 mAChR site, but the toxicological relevance and species and organ specificity of diethylphosphorylation are unknown.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • Blotting, Western
  • Chlorpyrifos / analogs & derivatives*
  • Chlorpyrifos / metabolism
  • Chlorpyrifos / toxicity*
  • Female
  • Insecticides / metabolism
  • Insecticides / toxicity*
  • Membrane Proteins / metabolism
  • Myocardium / metabolism*
  • Phosphorylation
  • Precipitin Tests
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, Muscarinic M2
  • Receptors, Muscarinic / immunology
  • Receptors, Muscarinic / metabolism*
  • Tritium

Substances

  • Antibodies, Monoclonal
  • Insecticides
  • Membrane Proteins
  • Receptor, Muscarinic M2
  • Receptors, Muscarinic
  • Tritium
  • O,O-diethyl O-3,5,6-trichloro-2-pyridyl phosphate
  • Chlorpyrifos