| Summary: | Copper (Cu<sup>2+</sup>) and zinc (Zn<sup>2+</sup>) are two kinds of heavy metals essential to living organisms. Cu<sup>2+</sup> and Zn<sup>2+</sup> at excessive concentrations can cause adverse effects on animals, but little is known about the thyroid-disrupting effects of these metals in fish, especially in the early developmental transition stage from embryos to larvae. Wild-type zebrafish embryos were used to expose to Cu<sup>2+</sup> (0, 1.5, 15, and 150 μg/L) and Zn<sup>2+</sup> (0, 20, 200, and 2000 μg/L) for 120 h. Thyroid hormone contents and transcriptional changes of the genes connected with the hypothalamic-pituitary-thyroid (HPT) axis were measured. Results showed that zebrafish embryos/larvae malformation rates were significantly increased in the Cu<sup>2+</sup> and Zn<sup>2+</sup> groups. Remarkably elevated thyroxine (T4) concentrations and reduced triiodothyronine (T3) concentrations were observed in Cu<sup>2+</sup> and Zn<sup>2+</sup> exposure fish. And the expression patterns of genes connected with the HPT axis were changed after Cu<sup>2+</sup> and Zn<sup>2+</sup> treatment. Based on principal component analysis (PCA) results, Zn<sup>2+</sup> caused significant effects on the thyroid endocrine system at 200 μg/L, while Cu<sup>2+</sup> resulted in thyroid disruption as low as 1.5 μg/L. In short, our study demonstrated that exposure to Cu<sup>2+</sup> and Zn<sup>2+</sup> induced developmental toxicity and thyroid disruption to zebrafish embryos/larvae.
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