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Main Title Neurotoxicity of Subchronic Acetylcholinesterase (AChE): Inhibition in Rat Hippocampus.
Author Veronesi, B. ; Jones, K. ; Pope, C. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Neurotoxicology Div.
Publisher c1990
Year Published 1990
Report Number EPA/600/J-90/122;
Stock Number PB91-109611
Additional Subjects Toxicology ; Cholinesterase inhibitors ; Acetylcholinesterase ; Hippocampus ; Insecticides ; Biochemistry ; Rats ; Nerve cells ; Pathology ; Nervous system ; Reprints ; Fenthion ; Binding sites ; Immunohistochemistry
Library Call Number Additional Info Location Last
NTIS  PB91-109611 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 19p
The neurotoxic effects of long term, low-level exposure to the commercially available insecticide, Fenthion, were examined in the present study. Young adult, male long-Evans rats were dermally exposed to Fenthion (25 mg/kg, 3X wk.) and sampled after 2 and 10 month exposure to assess neurotoxic damage in the hippocampus using morphological and biochemical endpoints. Cytopathology, consisting of gliosis and swollen and necrotic neurons, occurred in the dentate gyrus (DG) and hilus (CA4) as early as 2 mo. exposure. Acetylcholinesterase (AChE) staining of brain tissues taken at the time was severely reduced in the septal nuclei, the DG molecular layer, the hilus, and the hippocampus proper. After 10 mo. exposure to Fenthion, cellular necrosis and gliosis progressed to the CA3 regions and occasionally involved the CA2. Radiometric assays of AChE activity in the hippocampus indicated a 65% and 85% depression after 2 and 10 mo. exposure, respectively. Quinuclidinyl benzilate (QNB) binding for the hippocampal muscarinic receptor was reduced by 6% and 15% after 2 and 10 mo. exposure. A separate group of older (12 mo.) rats were exposed to the same dosing regimen of Fenthion and examined for neuropathic damage after 2 mo. and 10 mo. exposure. Aged animals exposed for only 2 mo. expressed severe hippocampal degeneration in a pattern similar to that seen in the young adult after 10 mo. exposure (viz., DG, CA4, CA3). (Copyright (c) 1990 by Academic Press, Inc.).