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Prenatal exposure to PFOS caused mitochondia-mediated apoptosis in heart of weaned rat

Authors

  • Huai-cai Zeng,

    1. Post-Doctoral Mobile Stations for Basic Medicine, University of South China, Hengyang, People's Republic of China
    2. Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China
    3. Institute of Pathogenic Biology, Medical College, University of South China, Hengyang, People's Republic of China
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    • These authors contributed equally to this work.

  • Qing-zhi He,

    1. Institute of Pathogenic Biology, Medical College, University of South China, Hengyang, People's Republic of China
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    • These authors contributed equally to this work.

  • Yuan-yuan Li,

    1. Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China
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  • Cheng-qiu Wu,

    1. Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China
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  • Yi-mou Wu,

    Corresponding author
    1. Institute of Pathogenic Biology, Medical College, University of South China, Hengyang, People's Republic of China
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  • Shun-qing Xu

    Corresponding author
    1. Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China
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ABSTRACT

Perfluorooctanyl sulfonate (PFOS), a cardiac toxicity compound, has been widely detected in the environment and in organisms. However, the toxic mechanism is not clear. Our previous study indicated that prenatal PFOS exposure led to swollen mitochondrial with vacuolar structure and loss of cristae in offsping's heart. The purpose of this study was to investigate the effect of PFOS on the apoptosis in developing heart and mitochondria-mediated apoptosis pathway. Pregnant Sprague-Dawley (SD) rats were exposed to PFOS at doses of 0.1, 0.6, and 2.0 mg/kg-d and 0.05% Tween 80 as control by gavage from gestation day 2 (GD 2) to GD 21. Apoptosis, as well as expression of apoptosis related genes associated with mitochondrial-mediated apoptosis pathway, including p53, bcl-2, bax, cytochrome c, caspase-9, and caspase-3 were analyzed in heart tissues from weaned (postnatal day 21, PND 21) offspring. The results showed that prenatal PFOS exposure resulted in apoptosis in the offspring's heart. The mRNA and protein expression levels of p53, bax, cytochrome c, caspase-9, and caspase-3 in the offspring's heart were enhanced in various PFOS-treated groups, meanwhile, the bcl-2 expression levels were decreased. Our results indicated that prenatal PFOS exposure induced the apoptosis of weaned offspring rat heart tissue via mitochondria-mediated apoptotic pathway. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1082–1090, 2015.

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