PUBLICATION
Effects of ZnO nanoparticles on perfluorooctane sulfonate induced thyroid-disrupting on zebrafish larvae
- Authors
- Du, J., Wang, S., You, H., Liu, Z.
- ID
- ZDB-PUB-160907-8
- Date
- 2016
- Source
- Journal of environmental sciences (China) 47: 153-64 (Journal)
- Registered Authors
- Keywords
- HPT axis, PFOS, nano-ZnO, thyroid hormone, zebrafish
- MeSH Terms
-
- Alkanesulfonic Acids/chemistry
- Alkanesulfonic Acids/toxicity*
- Animals
- Fluorocarbons/chemistry
- Fluorocarbons/toxicity*
- Nanoparticles/chemistry*
- Thyroid Gland/drug effects*
- Thyroid Gland/metabolism
- Triiodothyronine/metabolism
- Water Pollutants, Chemical/chemistry
- Water Pollutants, Chemical/toxicity*
- Zebrafish
- Zinc Oxide/chemistry*
- PubMed
- 27593282 Full text @ J. Environ. Sci. (China).
Citation
Du, J., Wang, S., You, H., Liu, Z. (2016) Effects of ZnO nanoparticles on perfluorooctane sulfonate induced thyroid-disrupting on zebrafish larvae. Journal of environmental sciences (China). 47:153-64.
Abstract
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, 0.8mg/L) and nano-ZnO (50mg/L) from their early stages of life (0-14days). 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 (0.8mg/L) and nano-ZnO (50mg/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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping