Carbaryl-induced elevation of corticosterone level and cholinergic mechanism.
Administration of a single dose (200 mg/kg, p.o.) of carbaryl to rats produced a significant rise in adrenal and plasma corticosterone levels and an increase of tyrosine alpha-ketoglutarate transaminase activity in the liver cytosol. Synaptosomal acetylcholinesterase activity of the hypothalamic and the striatal regions of rat brain was decreased by carbaryl treatment under similar conditions. Pretreatment (0.5 h) with atropine sulphate (10 mg/kg, i.p.) failed to counteract the carbaryl-induced elevation of adrenal and plasma corticosterone levels and hence the liver tyrosine alpha-ketoglutarate transaminase activity. Present results suggest that the carbaryl-induced rise in the corticosterone level in the adrenal gland and plasma is not due to a cholinergic mechanism.
D000302:Adrenal Cortex / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D012721:Carbaryl / Q000494:pharmacology*; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D003342:Corpus Striatum / Q000201:enzymology; D003345:Corticosterone / Q000378:metabolism*; D007031:Hypothalamus / Q000201:enzymology; D008297:Male; D051381:Rats; D013574:Synaptosomes / Q000201:enzymology; D014444:Tyrosine Transaminase / Q000378:metabolism
D002800:Cholinesterase Inhibitors; D001285:Atropine; D014444:Tyrosine Transaminase; D012721:Carbaryl; D003345:Corticosterone