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

被引：70
|
作者：
Chen, Tian [1 ]
Zhang, Ling [1 ,2 ]
Yue, Jun-qiu [3 ]
Lv, Zi-quan [1 ]
Xia, Wei [1 ]
Wan, Yan-jian [1 ]
Li, Yuan-yuan [1 ]
Xu, Shun-qing [1 ]
机构：
[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth, Minist Educ,Key Lab Environm & Hlth, Wuhan 430030, Peoples R China
[2] Wuhan Univ Sci & Technol, Coll Med, Dept Prevent Med, Wuhan 430065, Peoples R China
[3] Hubei Canc Hosp, Dept Pathol, Wuhan 430079, Peoples R China
来源：
REPRODUCTIVE TOXICOLOGY | 2012年 / 33卷 / 04期
基金：
中国国家自然科学基金;
关键词：
Perfluorooctane sulfonate; Prenatal; Lung; Oxidative stress; Apoptosis; PERFLUOROOCTANE SULFONATE PFOS; CELL-DEATH; PERFLUORINATED COMPOUNDS; DEVELOPMENTAL TOXICITY; PERFLUOROALKYL ACIDS; CIGARETTE-SMOKE; PREGNANCY; PATHWAYS; INJURY; MOUSE;
D O I：
10.1016/j.reprotox.2011.03.003
中图分类号：
Q [生物科学];
学科分类号：
07 ; 0710 ; 09 ;
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. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码：538 / 545
页数：8
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