Prenatal PFOS exposure induces oxidative stress and apoptosis in the lung of rat off-spring
Prenatal PFOS exposure induces oxidative stress and apoptosis in the lung of rat off-spring
复制标题
产前 PFOS 暴露诱导大鼠后代肺氧化应激和细胞凋亡
DOI：
10.1016/j.reprotox.2011.03.003
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发表时间：
2012-07-01
影响因子：
3.3
通讯作者：
Xu, Shun-qing
中科院分区：
文献类型：
--
作者：
Chen, Tian;Zhang, Ling;Xu, Shun-qing
全氟辛烷磺酸(PFOS)可引起啮齿动物新生鼠肺损伤。这项研究的目的是调查潜在的行动模式。孕鼠于妊娠第1~21天灌胃全氟辛烷磺酸(0、0.1、2.0 mg/kg·d)。对出生后0天(PND)和21只仔鼠的肺标本进行了全氟辛烷磺酸的毒性分析。结果表明，母鼠暴露于d全氟辛烷磺酸2.0 mg/kg后，子代肺组织出现严重的组织病理学改变，并伴有明显的氧化损伤和细胞凋亡，同时Bax/Bcl2比值、细胞色素c(Cytc)从线粒体向胞浆的释放、Fas和Fas-L的表达以及caspase-3、-8和-9的活性相应上调。结果表明，氧化应激以及内源性和外源性细胞死亡途径参与了全氟辛烷磺酸暴露所致的出生后肺损伤。(C)2011 Elsevier Inc.保留所有权利。
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. (C) 2011 Elsevier Inc. All rights reserved.