Perfluorooctane sulfonate（PFOS） and ZnO nanoparticles（nano-ZnO） are widely distributed in the environment.However,the potential toxicity of co-exposure to PFOS and nano-ZnO remains to be fully elucidated.The test ...Perfluorooctane sulfonate（PFOS） and ZnO nanoparticles（nano-ZnO） are widely distributed in the environment.However,the potential toxicity of co-exposure to PFOS and nano-ZnO remains to be fully elucidated.The test investigated the effects of co-exposure to PFOS and nano-ZnO on the hypothalamic–pituitary–thyroid（HPT） axis in zebrafish.Zebrafish embryos were exposed to a combination of PFOS（0.2,0.4,0.8 mg/L） and nano-ZnO（50 mg/L）from their early stages of life（0–14 days）.The whole-body content of TH and the expression of genes and proteins related to the HPT axis were analyzed.The co-exposure decreased the body length and increased the malformation rates compared with exposure to PFOS alone.Co-exposure also increased the triiodothyronine（T3） levels,whereas the thyroxine（T4）content remained unchanged.Compared with the exposure to PFOS alone,exposure to both PFOS（0.8 mg/L） and nano-ZnO（50 mg/L） significantly up-regulated the expression of corticotropin-releasing factor,sodium/iodidesymporter,iodothyronine deiodinases and thyroid receptors and significantly down-regulated the expression of thyroid-stimulating hormone,thyroglobulin（TG）,transthyretin（TTR） and thyroid receptors.The protein expression levels of TG and TTR were also significantly down-regulated in the co-exposure groups.In addition,the expression of the thyroid peroxidase gene was unchanged in all groups.The results demonstrated that PFOS and nano-ZnO co-exposure could cause more serious thyroid-disrupting effects in zebrafish than exposure to PFOS alone.Our results also provide insight into the mechanism of disruption of the thyroid status by PFOS and nano-ZnO.展开更多
基金supported by the State Key Laboratory of Urban Water Resource and Environment(Harbin Institute of Technology)(No.2013DX09)
文摘Perfluorooctane sulfonate（PFOS） and ZnO nanoparticles（nano-ZnO） are widely distributed in the environment.However,the potential toxicity of co-exposure to PFOS and nano-ZnO remains to be fully elucidated.The test investigated the effects of co-exposure to PFOS and nano-ZnO on the hypothalamic–pituitary–thyroid（HPT） axis in zebrafish.Zebrafish embryos were exposed to a combination of PFOS（0.2,0.4,0.8 mg/L） and nano-ZnO（50 mg/L）from their early stages of life（0–14 days）.The whole-body content of TH and the expression of genes and proteins related to the HPT axis were analyzed.The co-exposure decreased the body length and increased the malformation rates compared with exposure to PFOS alone.Co-exposure also increased the triiodothyronine（T3） levels,whereas the thyroxine（T4）content remained unchanged.Compared with the exposure to PFOS alone,exposure to both PFOS（0.8 mg/L） and nano-ZnO（50 mg/L） significantly up-regulated the expression of corticotropin-releasing factor,sodium/iodidesymporter,iodothyronine deiodinases and thyroid receptors and significantly down-regulated the expression of thyroid-stimulating hormone,thyroglobulin（TG）,transthyretin（TTR） and thyroid receptors.The protein expression levels of TG and TTR were also significantly down-regulated in the co-exposure groups.In addition,the expression of the thyroid peroxidase gene was unchanged in all groups.The results demonstrated that PFOS and nano-ZnO co-exposure could cause more serious thyroid-disrupting effects in zebrafish than exposure to PFOS alone.Our results also provide insight into the mechanism of disruption of the thyroid status by PFOS and nano-ZnO.
