Exposure to acrylamide inhibits uterine decidualization via suppression of cyclin D3/p21 and apoptosis in mice.

ABSTRACT

Acrylamide (ACR), a neurotoxicity and carcinogenic chemical, has attracted considerable attention since it is present at high concentrations in thermally cooked carbohydrate-rich foods. ACR exposure significantly increased rate of fetal resorption, and decreased fetal body weights in mice. However, no detailed information is available about the effect of ACR on uterine decidualization, which is a vital process in the establishment of successful pregnancy. Thus, our aim of this study was to explore the effect and mechanism of ACR on uterine decidualization in vivo during mice pregnancy. Mice were gavaged with 0, 10, and 50 mg ACR /kg/day from gestational days (GD) 1 until GD 8, whereas pseudopregnant mice from pseudopregnant day (PPD) 4 until PPD 8. Results indicated ACR treatment dramatically reduced numbers of implanted embryos, and decreased the weights of implantation site and oil-induced uterus. Nevertheless, no significant difference was observed in the weights of no oil-induced uterus between control and ACR-treated group. Furthermore, ACR significantly reduced numbers of polyploidy and PCNA-positive decidual cells and expression of cyclin D3 and p21 proteins, and induced apoptosis of decidua, as presented by up-regulation of Bax and cleaved-caspase-3, and decreased Bcl-2 protein during normal pregnant and pseudopregnant process. In summary, ACR exposure significantly inhibited uterine endometrial decidualization via the apoptosis and suppression of cyclin D3/p21 in mice.