Paraoxon toxicity is not potentiated by prior reduction in blood acetylcholinesterase

Toxicol Appl Pharmacol. 1992 Nov;117(1):110-5. doi: 10.1016/0041-008x(92)90224-g.

Abstract

The role of blood acetylcholinesterase in moderating the effects of organophosphate challenge in rats was tested. Adult male rats (n = 42) were injected (iv) either with monoclonal antibodies (MAb) to rat acetylcholinesterase (EC 3.1.1.7; AChE) or normal mouse IgG (controls). Two days later, the rats were injected (sc) with either a mild (0.17 mg/kg) or moderate dosage (0.34 mg/kg) of paraoxon or with vehicle. Neurological integrity was assessed by a functional observational battery followed by motor activity, 3 to 4 hr after dosing. Blood, brain, and diaphragm tissues were then collected for determination of AChE activity. MAb treatment reduced whole blood and plasma AChE activity by 32 and 90%, respectively, but did not affect neurobehavioral parameters or the AChE activity of brain or diaphragm. The paraoxon challenge produced dose-related neurobehavioral changes and inhibition of brain and diaphragm AChE activity to the same extent in IgG- and MAb-treated rats. Thus, significant loss in blood AChE alone produced no detectable neurobehavioral deficits and did not alter the subsequent responses to paraoxon challenge.

Publication types

  • Comparative Study

MeSH terms

  • Acetylcholinesterase / blood*
  • Acetylcholinesterase / immunology
  • Acetylcholinesterase / physiology
  • Animals
  • Antibodies, Monoclonal
  • Behavior, Animal / drug effects
  • Brain / enzymology
  • Diaphragm / enzymology
  • Drug Synergism
  • Male
  • Mice
  • Motor Activity / drug effects
  • Paraoxon / toxicity*
  • Rats
  • Rats, Sprague-Dawley
  • Sensitivity and Specificity

Substances

  • Antibodies, Monoclonal
  • Acetylcholinesterase
  • Paraoxon