| Perfluorinated compounds (PFCs) are a new type of persistent organic pollutants (POPs) with high-energy carbon-fluorine (C-F) bond and of concern due to their wide occurrence in the environment and potential adverse effects on wild life and human. While previous studies focused on PFOA and PFOS, the information on perfluorotridecanoate acid (PFTriDA), a longer-chain perfluorinated carboxylic acid (PFCA), including tissue distribution, bioconcentration and toxic effects was limited which has been widely detected in environment and wildlife in recent years . This study used model animal medaka (Oryzias Latipes) to investigate the tissue distribution, bioconcentration and the long-term chronic toxic effects of PFTriDA in their full life stages. The main results are as follows:(1) We have assessed the tissue distribution and bioconcentration in the medaka exposed to different concentrations of PFTriDA. The highest concentration of PFTriDA was detected in gonad, followed by egg, liver and carcass, which was similar to the tissue distribution in wild Chinese Sturgeon (Acipenser sinensis) except for gonad. For all tissues, male accumulated higher concentrations than female, which was demonstrated to be mainly due to high maternal transfer efficiency in adult female by bioenergenetic model. The bioconcentration factor (BCF) was found to be decreased with increasing the exposure concentration of PFTriDA.(2) To investigate the effects of prolonged exposure to PFTriDA on reproduction and development, medaka were exposed to PFTriDA from 0 day post-hatching to breeding age, persist for 80 days, and the impacts on embryonic development of F1 were also assessed. The results showed that PFTriDA exposure significantly induced the development of liver and gonad of female medaka in 0.2, 1 and 5μg/L groups, but did not affect the weight, length and condition factor (K) as well as male medaka. Egg production was inhibited with increasing exposure concentrations of PFTriDA, but the number of egg in 50μg/L group was not the least. In addition, impaired F1 embryonic development and severe developmental malformation such as conjoined twins and curled tail were observed in PFTriDA exposure groups, while the fertilization rate, hatching rate and hatching time of F1 embryos was not affected.(3) Based on the results of reproduction and development toxicity of PFTriDA, we investigated the hepatotoxicity of PFTriDA. Although no obvious histological damage of liver, the oxidative damage induced by long-term exposure to PFTriDA in male medaka was slightly obvious than female, but the expressions of the purpose genes on fatty acid metabolism were not affected. Up-regulation of P53 in medaka has relation with apoptosis and embryonic deformity. Maybe it is the low concentrations of PFTriDA exposure that medaka did not perform obvious hepatotoxicity.(4) To investigate the mechanisms underlining the declined reproductive success, the endocrine disruption of PFTriDA exposure to medaka was assessed. Long-term exposure to PFTriDA did not influence the transcriptional expression of Vtg, but significantly inhibited the expressions of StAR, Cyp11a, HSD-17βand Cyp19 involved in steroid hormone synthesis pathway, indicating that PFTriDA exposure has inhibitory effect to HPG (Hypothalamic-Pituitary-Gonadal axis). Exposure to PFTriDA on the gene expression involved in thyroid metabolism pathway was further assessed. The expression of TTR was increased in 0.2 and 1μg/L groups, and decreased in 5 and 50μg/L groups, indicating PFTriDA exposure could induce the release of thyroxine from thyroid follicles in lower exposure concentrations groups, and opposite in higher groups. In addition, PFTriDA exposure inhibited the expression of Ugt2A1. In conclusion, long-term exposure to PFTriDA disrupted endocrine system, and influenced the reproductive success of adults. |
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