||Fenthion Produces a Persistent Decrease in Muscarinic Receptor Function in the Adult Rat Retina.
Tandon, P. ;
Padilla, S. ;
Barone, S. ;
Pope, C. N. ;
Tilson, H. A. ;
||North Carolina Univ. at Chapel Hill. Center for Environmental Medicine and Lung Biology. ;ManTech Environmental Technology, Inc., Research Triangle Park, NC. ;Northeast Louisiana Univ., Monroe. School of Pharmacy.;Health Effects Research Lab., Research Triangle Park, NC. Neurotoxicology Div.
||EPA-68-D2-0056, EPA-817643-01-0; EPA/600/J-94/518;
Muscarinic receptors ;
Cholinesterase inhibitors ;
Signal transduction ;
Inositol phosphates ;
Quinuclidinyl benzilate ;
Glial fibrillary acidic protein ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
Several reports have suggested that exposure to organophosphate pesticides damages the visual system. The prolonged effects of an acute dose of fenthion (dimethyl 3-methyl-4-methylthiophenyl phosphorothionate) were studied on the cholinergic system of the rat retina. Fenthion was administered in a single dose of 0 or 100 mg/kg (sc, in corn oil) to adult, male, Long-Evans rats. The animals were killed 4, 14, or 56 days after treatment and cholinesterase (ChE) activity as well as muscarinic receptor (mChR) function measured in the retina and frontal cortex. Fenthion produced 89% inhibition of ChE activity in both tissues at 4 days, and, although there was recovery, slight (15%) inhibition of the enzyme activity was still observed at 56 days in both tissues. A long-lasting decrease in carbachol-stimulated inositolphosphate (IP) release was observed following fenthion treatment in the retina: IP release was depressed at 4 days and this depression persisted up to 56 days after dosing. The density of mChR in the retina as well as in the cortex was decreased by 14-20% at 4 days and returned to control levels by 56 days. (Copyright (c) 1994 by Academic Press, Inc.)