Possible involvement of beta-adrenergic receptors in the enhancement of nocturnal pineal N-acetyltransferase activity due to parathion administration.
The purpose of the present study was to examine the effects of administration of sublethal doses of O,O-diethyl-O-p-nitrophenyl phosphorothioate (parathion) on serum epinephrine (EPI) and norepinephrine (NE), as well as on night-time rat pineal melatonin synthesis, both in the presence and absence of propranolol, a beta-adrenergic receptor antagonist. In the first experiment, two groups of adult albino rats were administered parathion orally (1.08 and 2.17 mg/kg/day; the total received by each animal was 6.5 and 13.0 mg/kg body weight over 6 days); another two groups received corn oil only. Animals were killed at 23:00 and 01:00 h by decapitation. Serum EPI was augmented at 01:00 h, but NE was increased at 01:00 and 23:00 h due to administration of the high dose of parathion (13 mg/kg). In the second experiment, two groups of adult male albino rats were administered parathion orally (13 mg/kg); another two groups received an intraperitoneal injection of propranolol (20 mg/kg body weight, 1 h before the lights were turned off). In addition, two groups were given a saline injection. Four hours after darkness onset, pineal N-acetyltransferase (NAT) activity as well as pineal and serum melatonin levels were measured. Parathion by itself significantly augmented nocturnal pineal NAT activity and serum melatonin levels in otherwise untreated rats; the insecticide was ineffective in reference to this enzyme when it was given in conjunction with the beta-adrenergic receptor antagonist propranolol. The augmentation of NAT activity by parathion also caused significant reduction in pineal serotonin (5-HT); again, this response was blocked by propranolol treatment. The results are consistent with the idea that parathion influences pineal 5-HT metabolism either at the level of the beta-adrenergic receptor or via the sympathetic innervation to the pineal gland.
Attia
A M
AM
Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria, Egypt.
D000818:Animals; D001191:Arylamine N-Acetyltransferase / Q000378:metabolism*; D002940:Circadian Rhythm; D007306:Insecticides / Q000633:toxicity*; D008297:Male; D008550:Melatonin / Q000096:biosynthesis; D009638:Norepinephrine / Q000097:blood; D010278:Parathion / Q000633:toxicity*; D010870:Pineal Gland / Q000187:drug effects* / Q000201:enzymology; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D012701:Serotonin / Q000378:metabolism
D007306:Insecticides; D011943:Receptors, Adrenergic, beta; D012701:Serotonin; D010278:Parathion; D001191:Arylamine N-Acetyltransferase; D008550:Melatonin; D009638:Norepinephrine