Abstract
Copper (Cu(2+)) and zinc (Zn(2+)) are two kinds of heavy metals essential to living organisms. Cu(2+) and Zn(2+) 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(2+) (0, 1.5, 15, and 150 μg/L) and Zn(2+) (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(2+) and Zn(2+) groups. Remarkably elevated thyroxine (T4) concentrations and reduced triiodothyronine (T3) concentrations were observed in Cu(2+) and Zn(2+) exposure fish. And the expression patterns of genes connected with the HPT axis were changed after Cu(2+) and Zn(2+) treatment. Based on principal component analysis (PCA) results, Zn(2+) caused significant effects on the thyroid endocrine system at 200 μg/L, while Cu(2+) resulted in thyroid disruption as low as 1.5 μg/L. In short, our study demonstrated that exposure to Cu(2+) and Zn(2+) induced developmental toxicity and thyroid disruption to zebrafish embryos/larvae.