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Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay

Perfluorooctanesulfonate (PFOS) has been widely detected in the environment, wildlife and humans, but few studies have ever examined its mutagenic effect in vivo. In the present study, we use a transgenic fish model, the λ transgenic medaka, to evaluate the potential mutagenicity of PFOS in vivo fol...

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Autores principales: Chen, Yuanhong, Hu, Wei, Huang, Changjiang, Hua, Shushan, Wei, Qihao, Bai, Chenglian, Chen, Jiangfei, Norris, Michelle B., Winn, Richard, Yang, Dongren, Dong, Qiaoxiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5144067/
https://www.ncbi.nlm.nih.gov/pubmed/27929129
http://dx.doi.org/10.1038/srep38466
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author Chen, Yuanhong
Hu, Wei
Huang, Changjiang
Hua, Shushan
Wei, Qihao
Bai, Chenglian
Chen, Jiangfei
Norris, Michelle B.
Winn, Richard
Yang, Dongren
Dong, Qiaoxiang
author_facet Chen, Yuanhong
Hu, Wei
Huang, Changjiang
Hua, Shushan
Wei, Qihao
Bai, Chenglian
Chen, Jiangfei
Norris, Michelle B.
Winn, Richard
Yang, Dongren
Dong, Qiaoxiang
author_sort Chen, Yuanhong
collection PubMed
description Perfluorooctanesulfonate (PFOS) has been widely detected in the environment, wildlife and humans, but few studies have ever examined its mutagenic effect in vivo. In the present study, we use a transgenic fish model, the λ transgenic medaka, to evaluate the potential mutagenicity of PFOS in vivo following a subchronic exposure of 30 days. The mutant frequency of cII target gene was 3.46 × 10(−5) in liver tissue from control fish, which increased by 1.4-fold to 4.86 × 10(−5) in fish exposed to 6.7 μg/L PFOS, 1.55-fold to 5.36 × 10(−5) in fish exposed to 27.6 μg/L PFOS, and 2.02-fold to 6.99 × 10(−5) in fish exposed to 87.6 μg/L PFOS. This dose-dependent increase of mutant frequency was also accompanied with mutational spectrum changes associated with PFOS exposure. In particular, PFOS-induced mutation was characterized by +1 frameshift mutations, which increased from 0% in control fish to 13.2% in fish exposed to 27.6 μg/L PFOS and 14.6% in fish exposed to 87.6 μg/L PFOS. Our findings provide the first evidence of PFOS’s mutagenicity in an aquatic model system. Given the fact that most conventional mutagenic assays were negative for PFOS, we propose that PFOS-induced mutation in liver tissue of λ transgenic medaka may be mediated through compromised liver function.
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spelling pubmed-51440672016-12-16 Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay Chen, Yuanhong Hu, Wei Huang, Changjiang Hua, Shushan Wei, Qihao Bai, Chenglian Chen, Jiangfei Norris, Michelle B. Winn, Richard Yang, Dongren Dong, Qiaoxiang Sci Rep Article Perfluorooctanesulfonate (PFOS) has been widely detected in the environment, wildlife and humans, but few studies have ever examined its mutagenic effect in vivo. In the present study, we use a transgenic fish model, the λ transgenic medaka, to evaluate the potential mutagenicity of PFOS in vivo following a subchronic exposure of 30 days. The mutant frequency of cII target gene was 3.46 × 10(−5) in liver tissue from control fish, which increased by 1.4-fold to 4.86 × 10(−5) in fish exposed to 6.7 μg/L PFOS, 1.55-fold to 5.36 × 10(−5) in fish exposed to 27.6 μg/L PFOS, and 2.02-fold to 6.99 × 10(−5) in fish exposed to 87.6 μg/L PFOS. This dose-dependent increase of mutant frequency was also accompanied with mutational spectrum changes associated with PFOS exposure. In particular, PFOS-induced mutation was characterized by +1 frameshift mutations, which increased from 0% in control fish to 13.2% in fish exposed to 27.6 μg/L PFOS and 14.6% in fish exposed to 87.6 μg/L PFOS. Our findings provide the first evidence of PFOS’s mutagenicity in an aquatic model system. Given the fact that most conventional mutagenic assays were negative for PFOS, we propose that PFOS-induced mutation in liver tissue of λ transgenic medaka may be mediated through compromised liver function. Nature Publishing Group 2016-12-08 /pmc/articles/PMC5144067/ /pubmed/27929129 http://dx.doi.org/10.1038/srep38466 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Chen, Yuanhong
Hu, Wei
Huang, Changjiang
Hua, Shushan
Wei, Qihao
Bai, Chenglian
Chen, Jiangfei
Norris, Michelle B.
Winn, Richard
Yang, Dongren
Dong, Qiaoxiang
Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay
title Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay
title_full Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay
title_fullStr Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay
title_full_unstemmed Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay
title_short Subchronic perfluorooctanesulfonate (PFOS) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay
title_sort subchronic perfluorooctanesulfonate (pfos) exposure induces elevated mutant frequency in an in vivo λ transgenic medaka mutation assay
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5144067/
https://www.ncbi.nlm.nih.gov/pubmed/27929129
http://dx.doi.org/10.1038/srep38466
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