Record Display for the EPA National Library Catalog

RECORD NUMBER: 5 OF 17

OLS Field Name OLS Field Data
Main Title Cytogenetic Studies of Ethyl Acrylate Using C57BL/6 Mice.
Author Kligerman, A. D. ; Atwater, A. L. ; Bryant, M. F. ; Erexson, G. L. ; Kwanyuen., P. ;
CORP Author Environmental Health Research and Testing, Inc., Research Triangle Park, NC.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1991
Year Published 1991
Report Number EPA-68-02-4456; EPA/600/J-91/090;
Stock Number PB91-200246
Additional Subjects Chromosome aberrations ; Toxicology ; Mutagens ; In vivo analysis ; Dose-response relationships ; Cytochalasin B ; Sister chromatid exchange ; Mitosis ; Spleen ; Lymphocytes ; Micronucleus test ; Cell cycle ; Mice ; Reprints ; Ethyl acrylate
Holdings
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Status
NTIS  PB91-200246 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 09/04/1991
Collation 7p
Abstract
The clastogenicity of ethyl acrylate (EA) was examined in vivo by injecting i.p. 5 male C57BL/6 mice per dose group with either 125, 250, 500, 1000 mg/kg EA dissolved in saline. Twenty-four hours after injection, the animals were anesthetized, the spleens aseptically removed, and the splenic lymphocytes cultured for scoring chromosome aberrations (CAs) in first division cells and sister chromatid exchanges (SCEs) in second division cells. In the remaining cultures cytochalasin B was added to produce binucleated cells for scoring micronuclei (MN). There was no other significant increase in SCEs or CAs at any of the doses of EA examined. At the highest dose examined (1000 mg/kg), EA did cause a small but significant increase in binucleated cell MN. Isolated splenocytes were exposed to a wide range of concentrations of EA during the G(sub 0) stage of the cell cycle or 23 h after mitogen stimulation during the late G(sub 1) or early S-phrase of the cell cycle. Although EA was toxic for both exposure regimes, significant increases in chromatid-type aberrations were found only when the target cells were treated 23 h after mitogenic stimulation. No statistically-significant increase in SCE frequency was found after either treatment regime.