Developmental Toxicity and Thyroid-Disrupting Effects of Combined Exposure to Pb(II) and ²¹⁰Pb(II) in Zebrafish...

The toxicity of radioactive metals arises from both chemical toxicity and radiotoxicity. ²¹⁰Pb(II) is a long-lived radionuclide in the decay chain of natural uranium series ²³⁸U and exhibits extremely high toxicity. Both ²¹⁰Pb(II) and Pb(II) are widely present in natural water bodies. However, their combined toxicity remains unclear. Based on this, this study used zebrafish embryos as model organisms to investigate developmental toxicity, behavioral toxicity, and thyroid disruption effects, through single and combined exposure to Pb(II) (0, 1, 10, 100 μg/L) and ²¹⁰Pb(II) (0, 100, 1000 Bq/L) for 120 h by comparing the radiotoxicity of ²¹⁰Pb(II) with the chemical toxicity of Pb(II) and further exploring their combined effects. The results showed that following exposure to different environmental concentrations of Pb(II) and environmental activity levels of ²¹⁰Pb(II), exposure to Pb(II) alone caused an increase in the malformation rate of zebrafish embryos, a decrease in locomotor activity, and significant upregulation of thyroid-related genes, including thyroid hormone receptor beta (TRβ) and corticotropin-releasing hormone (CRH) in the larvae. Exposure to ²¹⁰Pb(II) alone had no significant effects on zebrafish embryos. Notably, compared with the individual exposure groups, the toxic effects in the combined exposure group of Pb(II) and ²¹⁰Pb(II) were further significantly enhanced. Furthermore, correlation analysis indicated a positive correlation between malformations in zebrafish embryos and the expression of key genes in the hypothalamic-pituitary-thyroid (HPT) axis. These findings suggest that under combined exposure, the chemical toxicity of Pb(II) plays a dominant role, while the radioactive component ²¹⁰Pb(II) exerts a synergistic amplification effect. This study provides important scientific evidence for improving the environmental risk assessment of radioactive metals.