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

Reprod Toxicol. 2012 Jul;33(4):538-545. doi: 10.1016/j.reprotox.2011.03.003. Epub 2011 Mar 31.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkanesulfonic Acids / toxicity*
  • Animals
  • Apoptosis / drug effects*
  • Blotting, Western
  • Cytochromes c / metabolism
  • Cytosol / metabolism
  • Environmental Pollutants / toxicity*
  • Female
  • Fluorocarbons / toxicity*
  • Gene Expression / drug effects
  • Gestational Age
  • In Situ Nick-End Labeling
  • Lung / drug effects*
  • Lung / metabolism
  • Lung / pathology
  • Maternal Exposure / adverse effects
  • Oxidative Stress / drug effects*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / chemically induced*
  • Prenatal Exposure Delayed Effects / metabolism
  • Prenatal Exposure Delayed Effects / pathology
  • Protein Transport
  • Rats, Sprague-Dawley
  • Real-Time Polymerase Chain Reaction


  • Alkanesulfonic Acids
  • Environmental Pollutants
  • Fluorocarbons
  • Cytochromes c
  • perfluorooctane sulfonic acid