Aim: Exposure to the ubiquitous endocrine disrupter Bisphenol A (BPA) has been associated, in pregnancy, with low birth weight. The aim of our study is the identification of the damage caused by Bisphenol A on placent...Aim: Exposure to the ubiquitous endocrine disrupter Bisphenol A (BPA) has been associated, in pregnancy, with low birth weight. The aim of our study is the identification of the damage caused by Bisphenol A on placental tissue through the evaluation of its effects on micro-vessel density and apoptosis. Methods: After fertilization, we exposed 3 female rats to oral BPA, by means of a free access to a beverage solution containing 100 μg/L of BPA. Three female rats were used as controls. Placentas underwent histological examination and immunohistochemistry for von Willebr and factor (F-VIII) and caspase-9. Results: Sixty-seven fetuses have been produced, 30 from control rats and 37 from exposed rats. Exposed fetuses showed a lower longitudinal/transverse diameter ratio than controls (2.57 ± 0.29 vs. 2.78 ± 0.38, p < 0.05). Also, exposed fetuses showed a significant reduction in the number of placental vessels per field (124.86 ± 19.15 vs. 143.54 ± 22.09, p < 0.05). On the other hand, apoptosis is not increased by exposure, as shown by caspase-9 levels. Conclusion: Exposure to BPA during pregnancy may affect placental vascularization, and this phenomenon may explain the lower birth weight reported. However, our results do not show the increase in apoptosis observed in vitro.展开更多
文摘Aim: Exposure to the ubiquitous endocrine disrupter Bisphenol A (BPA) has been associated, in pregnancy, with low birth weight. The aim of our study is the identification of the damage caused by Bisphenol A on placental tissue through the evaluation of its effects on micro-vessel density and apoptosis. Methods: After fertilization, we exposed 3 female rats to oral BPA, by means of a free access to a beverage solution containing 100 μg/L of BPA. Three female rats were used as controls. Placentas underwent histological examination and immunohistochemistry for von Willebr and factor (F-VIII) and caspase-9. Results: Sixty-seven fetuses have been produced, 30 from control rats and 37 from exposed rats. Exposed fetuses showed a lower longitudinal/transverse diameter ratio than controls (2.57 ± 0.29 vs. 2.78 ± 0.38, p < 0.05). Also, exposed fetuses showed a significant reduction in the number of placental vessels per field (124.86 ± 19.15 vs. 143.54 ± 22.09, p < 0.05). On the other hand, apoptosis is not increased by exposure, as shown by caspase-9 levels. Conclusion: Exposure to BPA during pregnancy may affect placental vascularization, and this phenomenon may explain the lower birth weight reported. However, our results do not show the increase in apoptosis observed in vitro.
