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Thyroid-Disrupting Effects of Cadmium and Mercury in Zebrafish Embryos/Larvae
Cadmium (Cd2+) and mercury (Hg2+) are two kinds of non-essential heavy metals. Cd2+ and Hg2+ can cause thyroid disruption, but very few researchers have investigated the thyroid-disrupting effects of these metals on fish, specifically during their early developmental transition stage from embryos to larvae. In this study, wild-type zebrafish embryos were exposed to varying concentrations (contents) of Cd2+ (0, 10, 100, and 1000 μg/L) and Hg2+ (0, 0.1, 1, and 10 μg/L) for 120 h. Thereafter, the thyroid hormone contents and transcriptional changes in the genes, including thyroid stimulating hormone-β (tshβ), thyroglobulin (tg), sodium-iodide symporter (nis), thyroid peroxidase (tpo), transthyretin (ttr), thyroid hormone receptor-α and -β (thrα, thrβ), types I and II iodothyronine deiodinase (dio1, dio2), and uridine diphosphate glucuronosyltransferase 1 family a, b (ugt1ab) associated with the hypothalamic-pituitary-thyroid (HPT) axis were measured. Results showed that zebrafish embryos/larvae malformation rates were significantly higher in the Cd2+ and Hg2+ groups. A significant increase in the thyroxine (T4) concentration and a decrease in the triiodothyronine (T3) concentration were observed in the Cd2+-exposed zebrafish embryos/larvae. On the other hand, the T4 and T3 concentrations were observed to be significantly increased after Hg2+ exposure. Additionally, changes were noted in the expression patterns of the HPT axis-linked genes after Cd2+ and Hg2+ exposure. Based on the results of the principal component analysis (PCA), it was concluded that Cd2+ exposure significantly affected the thyroid endocrine system at a concentration of 100 μg/L, whereas Hg2+ exposure led to a thyroid disruption at a low concentration of 0.1 μg/L. Thus, this study demonstrated that exposure to Cd2+ and Hg2+ metal ions induced developmental toxicity and led to thyroid disruption in zebrafish embryos/larvae.
Thyroid-Disrupting Effects of Cadmium and Mercury in Zebrafish Embryos/Larvae
Cadmium (Cd2+) and mercury (Hg2+) are two kinds of non-essential heavy metals. Cd2+ and Hg2+ can cause thyroid disruption, but very few researchers have investigated the thyroid-disrupting effects of these metals on fish, specifically during their early developmental transition stage from embryos to larvae. In this study, wild-type zebrafish embryos were exposed to varying concentrations (contents) of Cd2+ (0, 10, 100, and 1000 μg/L) and Hg2+ (0, 0.1, 1, and 10 μg/L) for 120 h. Thereafter, the thyroid hormone contents and transcriptional changes in the genes, including thyroid stimulating hormone-β (tshβ), thyroglobulin (tg), sodium-iodide symporter (nis), thyroid peroxidase (tpo), transthyretin (ttr), thyroid hormone receptor-α and -β (thrα, thrβ), types I and II iodothyronine deiodinase (dio1, dio2), and uridine diphosphate glucuronosyltransferase 1 family a, b (ugt1ab) associated with the hypothalamic-pituitary-thyroid (HPT) axis were measured. Results showed that zebrafish embryos/larvae malformation rates were significantly higher in the Cd2+ and Hg2+ groups. A significant increase in the thyroxine (T4) concentration and a decrease in the triiodothyronine (T3) concentration were observed in the Cd2+-exposed zebrafish embryos/larvae. On the other hand, the T4 and T3 concentrations were observed to be significantly increased after Hg2+ exposure. Additionally, changes were noted in the expression patterns of the HPT axis-linked genes after Cd2+ and Hg2+ exposure. Based on the results of the principal component analysis (PCA), it was concluded that Cd2+ exposure significantly affected the thyroid endocrine system at a concentration of 100 μg/L, whereas Hg2+ exposure led to a thyroid disruption at a low concentration of 0.1 μg/L. Thus, this study demonstrated that exposure to Cd2+ and Hg2+ metal ions induced developmental toxicity and led to thyroid disruption in zebrafish embryos/larvae.
Thyroid-Disrupting Effects of Cadmium and Mercury in Zebrafish Embryos/Larvae
Liqiao Zhong (author) / He Zhang (author) / Luyin Wu (author) / Huijun Ru (author) / Nian Wei (author) / Fan Yao (author) / Zhaohui Ni (author) / Xinbin Duan (author) / Yunfeng Li (author)
2022
Article (Journal)
Electronic Resource
Unknown
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