| First Author | Tan W | Year | 2013 |
| Journal | Toxicol Appl Pharmacol | Volume | 269 |
| Issue | 2 | Pages | 163-8 |
| PubMed ID | 23545179 | Mgi Jnum | J:197244 |
| Mgi Id | MGI:5491965 | Doi | 10.1016/j.taap.2013.03.016 |
| Citation | Tan W, et al. (2013) Bisphenol A differentially activates protein kinase C isoforms in murine placental tissue. Toxicol Appl Pharmacol 269(2):163-8 |
| abstractText | Bisphenol A is utilized to make polycarbonate plastics and is an environmental pollutant. Recent research has indicated that it is an endocrine disruptor and may interfere with reproductive processes. Our lab has previously shown that bisphenol A could regulate corticotrophin releasing hormone and aromatase in cultured placental cells. In the present study, the effect of bisphenol A on these two genes in the placenta was investigated in mice. Pregnant ICR mice were gavaged with bisphenol A at 2, 20 and 200mg/kg body weight/day from E13 to E16 and were euthanized at E17. Compared to the control mice, increased plasma estrogen and corticotrophin releasing hormone were observed in bisphenol A-treated mice. Messenger RNA quantification indicated that placental crh but not cyp19 was induced in mice treated with bisphenol A. Tracking the related signaling pathway, we found that protein kinase C zeta/lambda and delta were activated in the placentas of bisphenol A-treated mice. As the gene promoter of crh contains CRE and the half site of ERE, either phospho-PKC or estrogen could stimulate the gene transactivation. These results indicate that bisphenol A might increase plasma concentrations of estradiol, testosterone, corticotrophin releasing hormone and placental phospho-PKC zeta/lambda and delta in mice. Ultimately, the incidence of premature birth in these mice could increase. |
