Record Display for the EPA National Library Catalog

RECORD NUMBER: 21 OF 22

OLS Field Name OLS Field Data
Main Title Use of Glial Fibrillary Acidic Protein in First-Tier Assessments of Neurotoxicity.
Author O'Callaghan, J. P. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC.
Publisher 1991
Year Published 1991
Report Number EPA/600/D-91/050;
Stock Number PB91-191197
Additional Subjects Toxicology ; Nervous system ; Glial fibrillary acidic protein ; Toxic substances ; Brain chemistry ; Radioimmunoassay ; Dose-response relationships ; Cell survival ; Dopamine ; Tyrosine hydroxylase ; Enzyme-linked immunosorbent assay ; Astrocytes ;
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB91-191197 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 09/04/1991
Collation 29p
Abstract
Diverse neurotoxic insults result in proliferation and hypertrophy of astrocytes, a subtype of central nervous system glia. The hallmark of the response, often termed 'reactive gliosis', is the enhanced expression of the major intermediate filament protein of astrocytes, glial fibrillary acidic protein (GFAP). These morphological observations suggest that GFAP may be a useful biochemical indicator of neurotoxicity. To investigate the possibility the authors administered prototype neurotoxicants to experimental animals and then assessed the effects of these agents on the tissue content of GFAP, as determined by radioimmunoassay. The study found that assays of GFAP reveal dose- time- and region-dependent patterns of neurotoxicity at toxicant dosages below those that cause light microscopic evidence of cell loss or damage. No false positives have been seen following exposure to a variety of pharmacological agents. By using regional assessments of GFAP in a first-tier evaluation, it should be possible to localize areas of damage. A second-tier evaluation, using assays of proteins or transmitters associated with cells in the affected region, may reveal the cellular targets of neurotoxicity.