title: Hyperglycemic and stressogenic effects of monocrotophos in rats: evidence for the involvement of acetylcholinesterase inhibition.
abstract: The purpose of this study was to investigate the involvement of acetylcholinesterase (AChE) inhibition in hyperglycemic and stressogenic effects of monocrotophos in rats. Oral administration of monocrotophos (1.8 mg/kg b.w., 1/10 LD(50)) caused reversible hyperglycemia in rats with peak increase occurring at 2 h following administration. The hyperglycemic outcome at 2 h was accompanied by significant inhibition of acetylcholinesterase (AChE) activity in brain (84%), adrenal (68%) and liver (53%) and stressogenic effects as revealed by marked increase in plasma corticosterone (102%) and liver tyrosine aminotransferase (TAT) (104%) activity. At 4 h following administration, there was normalization of hyperglycemia and hypercorticosteronemia, marginal attenuation of liver TAT activity and marked increase in liver glycogen content, without spontaneous reactivation of AChE activity in the organs studied. Interestingly, pre-treatment of rats with acetylcholine (ACh) receptor antagonists-atropine sulfate and methyl atropine nitrate offered significant protection against hyperglycemia, hypercorticosteronemia and increased liver TAT activity induced by monocrotophos. Our results clearly demonstrate the involvement of AChE inhibition in hyperglycemia and stressogenic effects of monocrotophos in rats following acute exposure. Protection offered by both, general and peripheral ACh antagonists provide further evidence for the involvement of peripheral AChE inhibition in the monocrotophos-induced effects.
authors.affiliation: Food Protectants and Infestation Control Department, Central Food Technological Research Institute (CSIR Laboratory), Mysore 570020, India.
authors.forename: Apurva Kumar R
authors.initials: AK
authors.lastname: Joshi
authors.forename: P S
authors.initials: PS
authors.lastname: Rajini
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism*; D000311:Adrenal Glands / Q000187:drug effects / Q000201:enzymology; D000818:Animals; D001285:Atropine / Q000627:therapeutic use; D001286:Atropine Derivatives / Q000627:therapeutic use; D001786:Blood Glucose / Q000032:analysis; D001921:Brain / Q000187:drug effects / Q000201:enzymology; D018680:Cholinergic Antagonists / Q000627:therapeutic use; D002800:Cholinesterase Inhibitors / Q000633:toxicity*; D003345:Corticosterone / Q000097:blood; D006003:Glycogen / Q000378:metabolism; D006943:Hyperglycemia / Q000097:blood / Q000139:chemically induced* / Q000201:enzymology / Q000517:prevention & control; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008297:Male; D008999:Monocrotophos / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D011950:Receptors, Cholinergic / Q000378:metabolism; D013315:Stress, Psychological / Q000097:blood / Q000139:chemically induced* / Q000201:enzymology / Q000517:prevention & control; D014444:Tyrosine Transaminase / Q000378:metabolism
chemical_list: D001286:Atropine Derivatives; D001786:Blood Glucose; D018680:Cholinergic Antagonists; D002800:Cholinesterase Inhibitors; D011950:Receptors, Cholinergic; D008999:Monocrotophos; D001285:Atropine; C006649:methylatropine; D006003:Glycogen; D014444:Tyrosine Transaminase; D000110:Acetylcholinesterase; D003345:Corticosterone