| Literature DB >> 21440054 |
Tian Chen1, Ling Zhang2, Jun-Qiu Yue3, Zi-Quan Lv1, Wei Xia1, Yan-Jian Wan1, Yuan-Yuan Li1, Shun-Qing Xu4.
Abstract
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 2.0mg/kgd) 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 2.0mg/kgd 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.Entities:
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Year: 2011 PMID： 21440054 DOI： 10.1016/j.reprotox.2011.03.003
Source DB: PubMed Journal: Reprod Toxicol ISSN： 0890-6238 Impact factor: 3.143