Record Display for the EPA National Library CatalogRECORD NUMBER: 3 OF 3
|Main Title||Synaptonemal Complex Damage Induced by Clastogenic and Anti-Mitotic Chemicals: Implications for Non-Disjunction and Aneuploidy (Journal Version).|
|Author||Allen, J. W. ; Gibson, J. B. ; Poorman, P. A. ; Backer, L. C. ; Moses, M. J. ;|
|CORP Author||Health Effects Research Lab., Research Triangle Park, NC. Genetic Toxicology Div. ;Duke Univ. Medical Center, Durham, NC. ;Wellcome Research Labs., Research Triangle Park, NC.|
|Additional Subjects||Mutagens ; Toxicology ; Synopses ; Mice ; Laboratory animals ; Exposure ; Meiosis ; Mitomycins ; Cyclophosphamide ; Colchicine ; Chromosome abnormalities ; Reprints ; Aneuploidy ; Chromosomal translocation ; Genetic effects ; Mitomycin C ; Amsacrine ; Vinblastine sulfate ; Prophase ; Alkylating agents ; Chromosome breakage ; Toxic substances ; Sister chromatid exchanges ; Antimitotic drugs|
Mice were treated with mitomycin C, cyclophosphamide, amuscarine, colchicine, or vinblastine sulfate, and meiotic prophase cells analyzed for synaptonemal complex damage. All test agents caused synaptonemal complex breakage and synapsis irregularities, although propensities for inducing specific types of damage at S-phase or prophase stages varied among the chemicals. The data indicate that SC analysis can reveal chemical-specific alterations to meiotic homologue pairing/synapsis which have not generally been recognized, and which theoretically may be implicated in nondisjunction.