Chronic administration of an organophosphorus insecticide to rats alters cholinergic muscarinic receptors in the pancreas

Chemico-biological Interactions
L G CostaS D Murphy

Abstract

Male rats were treated for 10 days with the organophosphorus insecticide, acetylcholinesterase inhibitor, O,O-diethyl S-[2-(ethylthio)ethyl] phosphorodithioate (disulfoton, 2 mg/kg/day by gavage). At the end of the treatment, binding of [3H]quinuclidinyl benzilate ( [3H]QNB) to cholinergic muscarinic receptors and cholinesterase (ChE) activity were assayed in the pancreas. Functional activity of pancreatic muscarinic receptor was investigated by determining carbachol-stimulated secretion of alpha-amylase in vitro. ChE activity and [3H]QNB binding were significantly decreased in the pancreas from disulfoton-treated rats. The alteration of [3H]QNB binding was due to a decrease in muscarinic receptor density with no change in the affinity. Basal secretion of amylase from pancreas in vitro was not altered, but carbachol-stimulated secretion was decreased. The effect appeared to be specific since pancreozymin was able to induce the same amylase release from pancreases of control and treated rats. The results suggest that repeated exposures to sublethal doses of an organophosphorus insecticide lead to a biochemical and functional alteration of cholinergic muscarinic receptors in the pancreas.

References

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Jan 1, 1982·Toxicology·L G CostaS D Murphy
Jan 1, 1982·Pharmacology·I Lundquist
Jan 1, 1981·Toxicology·L G CostaS D Murphy
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Jul 1, 1961·Biochemical Pharmacology·G L ELLMANR M FEATHER-STONE

Citations

Aug 1, 1985·Journal of the Autonomic Nervous System·L G Costa, S D Murphy
Nov 2, 2013·Toxicologic Pathology·John R Foster
Nov 12, 2013·Drug Metabolism and Disposition : the Biological Fate of Chemicals·Feng LiXiaochao Ma

Related Concepts

Mégamylase
Metazoa
Carboptic
CCK-33
Cholase
Demeton
Insecticides
Pancreas
Quinuclidinyl Benzilate
August Rats

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