孕期全氟辛烷磺酸盐(PFOS)暴露诱导胎鼠肺损伤

Lung Impairments of Embryonic Rat Induced by Prenatal Perfluorooctane Sulfonate(PFOS) Exposure

为研究全氟辛烷磺酸盐(PFOS)暴露对胎鼠肺部损伤的诱导作用,孕期SD大鼠在5～20mg·kg-1剂量范围内的PFOS中处理7d,取胎鼠全肺并分析其发育所受的影响。通过形态学比较,发现随着PFOS浓度的增加,胎鼠体长和体重均显著降低,高剂量暴露会导致胎鼠死亡。通过组织学检测,发现胎鼠肺的发育受到PFOS暴露的抑制。通过WesternBlot检测肺泡Ⅰ/Ⅱ型细胞的发育,发现肺泡Ⅰ型细胞特异蛋白Podoplanin表达显著减少(p<0.05),肺泡Ⅱ型细胞特异蛋白SP-C表达减少但未出现显著差异,此外,与对照组相比高剂量暴露会引起血管内皮生长因子(VEGF)表达显著减少(p<0.01)。实验结果说明,PFOS暴露会导致胎鼠肺部发育出现损伤,这种损伤可能是肺泡Ⅰ型细胞及肺部血管发育受抑制引起胎鼠肺部气体交换功能破坏。

Perfluorooctane sulfonate （PFOS） exposure of pregnancy of SD rat inducing lung impairments of embryonic rat was studied. SD rats were exposed to PFOS at dosages from 5 mg kg 1 to 20 mg kg 1 for 7 days. The whole pups lung was collected and the developmental condition of lung was analyzed. Morphologi- caUy, the length and the weights of embryos significantly decreased after prenatal SD rats exposed to PFOS in a dose-dependent manner. Furthermore, higher dose PFOS caused death of embryonic rat. Histological obser- vation reveals that PFOS exposure inhibited the development of pups lung. Western Blot was used to detect the development of type I /II alveolar cell. Results showed that Podoplanin, or the specific protein of type I alveolar cell decreased significantly （p 〈0.05）, while SP-C, or the specific protein of type 1/ alveolar cell de- creased but not in a significant level. The vascular endothelial growth factor （VEGF） significantly decreased （p 〈0.01） in higher doses PFOS exposure compared with the control. Therefore, these results suggested that the mechanism on impairments of pups lung was probably induced by prenatal PFOS exposure impeding the de- velopment of type I alveolar cell and pulmonary vascellum, which damaged the pulmonary gas exchange.