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

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          Abstract

          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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          Most cited references32

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          Biological monitoring of polyfluoroalkyl substances: A review.

          Polyfluoroalkyl substances (PFSs) are used in industrial and commercial products and can degrade to persistent perfluorocarboxylates (PFCAs) and perfluoroalkyl sulfonates (PFSAs). Temporal trend studies using human, fish, bird, and marine mammal samples indicate that exposure to PFSs has increased significantly over the past 15-25 years. This review summarizes the biological monitoring of PFCAs, PFSAs, and related PFSs in wildlife and humans, compares concentrations and contamination profiles among species and locations, evaluatesthe bioaccumulation/biomagnification in the environment, discusses possible sources, and identifies knowledge gaps. PFSs can reach elevated concentrations in humans and wildlife inhabiting industrialized areas of North America, Europe, and Asia (2-30,000 ng/ mL or ng/g of wet weight (ww)). PFSs have also been detected in organisms from the Arctic and mid-ocean islands (< or = 3000 ng/g ww). In humans, PFSAs and PFCAs have been shown to vary among ethnic groups and PFCA/PFSA profiles differ from those in wildlife with high proportions of perfluorooctanoic acid and perfluorooctane sulfonate. The pattern of contamination in wildlife varied among species and locations suggesting multiple emission sources. Food web analyses have shown that PFCAs and PFSAs can bioaccumulate and biomagnify in marine and freshwater ecosystems. Knowledge gaps with respect to the transport, accumulation, biodegradation, temporal/spatial trends and PFS precursors have been identified. Continuous monitoring with key sentinel species and standardization of analytical methods are recommended.
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            Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype.

            Cancers of the microsatellite mutator phenotype (MMP) show exaggerated genomic instability at simple repeat sequences. More than 50 percent (21 out of 41) of human MMP+ colon adenocarcinomas examined were found to have frameshift mutations in a tract of eight deoxyguanosines [(G)8] within BAX, a gene that promotes apoptosis. These mutations were absent in MMP- tumors and were significantly less frequent in (G)8 repeats from other genes. Frameshift mutations were present in both BAX alleles in some MMP+ colon tumor cell lines and in primary tumors. These results suggest that inactivating BAX mutations are selected for during the progression of colorectal MMP+ tumors and that the wild-type BAX gene plays a suppressor role in a p53-independent pathway for colorectal carcinogenesis.
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              Microsatellite instability and mutations of the transforming growth factor beta type II receptor gene in colorectal cancer.

              The TGF beta type II receptor (RII) was found to be mutated within a polyadenine tract in 100 of 111 (90%) colorectal cancers with microsatellite instability. Other polyadenine tracts of similar length were mutated in these samples but not as frequently as RII. In most cases, the polyadenine tract mutations affected both alleles of RII, and in four tumors heterozygous for the polyadenine mutations, three had additional mutations that were expected to inactivate the other RII allele. These genetic data support the idea that RII behaves like a tumor suppressor during CR cancer development and is a critical target of inactivation in mismatch repair-deficient tumors.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                08 December 2016
                2016
                : 6
                : 38466
                Affiliations
                [1 ]Institute of Environmental Safety and Human Health, Wenzhou Medical University , Wenzhou 325035, P.R. China
                [2 ]Aquatic Biotechnology and Environmental Laboratory, Warnell School of Forest Resources, University of Georgia , Athens, Georgia, USA
                Author notes
                [*]

                These authors contributed equally to this work.

                Article
                srep38466
                10.1038/srep38466
                5144067
                27929129
                63d528d0-1bc6-4be8-a4b2-169c7f4a1df2
                Copyright © 2016, The Author(s)

                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/

                History
                : 14 January 2016
                : 09 November 2016
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