To examine the ability of estrogens and anti-estrogens to induce cellular transformation and genetic effects, Syrian hamster embryo (SHE) cells were treated with estrogens, 17beta-estradiol (E2) or diethylstilbestrol (DES), or with anti-estrogens, tamoxifen (TAM), toremifene (TOR) or ICI 164,384. Tr
Bisphenol-A induces cellular transformation, aneuploidy and DNA adduct formation in cultured Syrian hamster embryo cells
✍ Scribed by Takeki Tsutsui; Yukiko Tamura; Eiichi Yagi; Koko Hasegawa; Masayuki Takahashi; Noriko Maizumi; Fusae Yamaguchi; J. Carl Barrett
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- French
- Weight
- 90 KB
- Volume
- 75
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Bisphenol-A (BP
-A) is a major component of epoxy, polycarbonate and other resins. For an assessment of in vitro carcinogenicity and related activity of BP-A, the abilities of this compound to induce cellular transformation and genetic effects were examined simultaneously using the Syrian hamster embryo (SHE) cell model. Cellular growth was reduced by continuous treatment with BP-A at doses H100 M. However, colony-forming efficiencies were not decreased significantly following treatment with up to 200 M BP-A for 48 hr. Morphological transformation of SHE cells was induced by treatment of cells with BP-A at 50 to 200 M for 48 hr. BP-A exhibited transforming activity at doses H50 M but was less active than the benzo[␣]pyrene used as a positive control. Over the dose range that resulted in cellular transformation, treatment of SHE cells with BP-A failed to induce gene mutations at the Na ؉ /K ؉ ATPase locus or the hprt locus. No statistically significant numbers of chromosomal aberrations were detected in SHE cells treated with BP-A. However, treatment of cells with BP-A induced numerical chromosomal changes in the near diploid range at doses that induced cellular transformation. 32 P-Postlabeling analysis revealed that exposure of cells to BP-A also elicited DNA adduct formation in a dose-dependent fashion. Our results indicate that BP-A has cell-transforming and genotoxic activities in cultured mammalian cells and potential carcinogenic activity.
📜 SIMILAR VOLUMES
## Abstract To examine a possible mechanism of endogenous estrogen‐induced carcinogenesis, we studied the effect of the catechol‐__O__‐methyltransferase (COMT) inhibitor Ro 41‐0960 on cell transforming and clastogenic activities of 2 catechol estrogens 2‐ and 4‐hydroxyestrone (2‐ or 4‐OHE~1~) using
To examine a direct involvement of genotoxic effects of estrogens in the initiation of hormonal carcinogenesis, the abilities of 17beta-estradiol (E2) and 8 of its metabolites to induce cellular transformation and genetic effects were studied using the Syrian hamster embryo (SHE) cell model. Treatme