Prenatal PFOS exposure induces oxidative stress and apoptosis in the lung of rat off-spring

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• 作者：Tian Chen^a ; ¹ ; Ling Zhang^a ; ^b ; ¹ ; Jun-qiu Yue^c ; Zi-quan Lv^a ; Wei Xia^a ; Yan-jian Wan^a ; Yuan-yuan Li^a ; Shun-qing Xu^a ; ^{xuscience@hotmail.com}
• 关键词：Perfluorooctane sulfonate ; Prenatal ; Lung ; Oxidative stress ; Apoptosis
• 刊名：Reproductive Toxicology
• 出版年：2012
• 期刊代码：233_08906238
• 类别：med
• 出版时间：July, 2012
• 卷：33
• 期：4
• 页码：538-545
• 文件大小：1773 K

摘要

Perfluorooctane sulfonate (PFOS) could induce neonatal pulmonary injuries in rodents. The aim of this study was to investigate the underlying mode of action. Pregnant rats were dosed orally with PFOS (0, 0.1 and 2.0 mg/kg d) from gestation days (GD) 1 to 21. Lung samples from postnatal day (PND) 0 and 21 pups were analyzed for the toxic effects of PFOS. The results showed that maternal exposure to 2.0 mg/kg d PFOS caused severe histopathological changes along with marked oxidative injuries and cell apoptosis in offspring lungs; at the same time, the ratio of Bax to Bcl-2, release of cytochrome c (Cyt c) from mitochondria to cytoplasm, expressions of Fas and Fas-L, and activities of caspase-3, -8 and -9 were up-regulated correspondingly. The results indicate that oxidative stress and both intrinsic and extrinsic cell death pathways were involved in prenatal PFOS exposure-induced injuries in postnatal lungs.