||Paraoxon Toxicity Is Not Potentiated by Prior Reduction in Blood Acetylcholinesterase.
Padilla, S. ;
Moser, V. C. ;
Pope, C. N. ;
Brimijoin, W. S. ;
||Environmental Protection Agency, Research Triangle Park, NC. Neurotoxicology Div. ;ManTech Environmental Technology, Inc., Research Triangle Park, NC. ;Northeast Louisiana Univ., Monroe. Toxicology Program. ;Mayo Clinic, Rochester, MN. Dept. of Pharmacology.
Cholinesterase inhibitors ;
Monoclonal antibodies ;
Organophosphorus compounds ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
The role of blood acetylcholinesterase in moderating the effects of organophosphate challenge in rats were tested. Adult male rats (n=42) were injected (i.v.) either with monoclonal antibodies (MAb) to rat acetylcholinesterase (EC 188.8.131.52; AChE) or normal mouse IgG (controls). Two days later, the rats were injected (s.c.) with a mild dosage of paraoxon (0.17 mg/kg), a moderate dosage (0.34 mg/kg) or with vehicle. MAb treatment reduced whole blood and plasma AChE activity by 32% and 90%, respectively, but did not affect neurobehavioral parameters or the AChE activity of brain or diaphragm. The paraoxon challenge produced dose-related neurobehavioral changes and inhibition of brain and diaphragm AChE activity to the same extent in IgG and MAb treated rats. Thus, significant loss in blood AChE alone produced no detectable neurobehavioral deficits and did not alter the subsequent responses to paraoxon challenge.