Thyroid disruption and developmental toxicity caused by Cd2+ in Schizopygopsis younghusbandi larvae

Abstract

In recent years, the adverse effects of cadmium (Cd²⁺) on aquatic systems have attracted much attention because Cd²⁺ can induce endocrine disorders and toxicity in aquatic organisms at low levels. However, its effects on the thyroid system in native fish in Lhasa are still unclear. In the present study, Schizopygopsis younghusbandi larvae were exposed to Cd²⁺ (0.25, 2.5, 25 or 250 μg/L) for 7 or 14 days to determine its toxic effects on thyroid function. The results showed that whole-body total T4 and T3 levels were significantly decreased, which was accompanied by the significant upregulation of the expression of the dio1 and dio2 genes after exposure to Cd²⁺ for 7 or 14 days. Genes related to thyroid hormone synthesis (crh and tshβ) were upregulated after both 7 and 14 days of Cd²⁺ exposure, possibly due to the negative feedback regulation of the hypothalamic-pituitary-thyroid (HPT) axis caused by a decrease in thyroid hormone. In addition, survival rates and body lengths were reduced after treatment with Cd²⁺. This suggests that Cd²⁺ caused developmental toxicity in Schizopygopsis younghusbandi larvae. An integrated assessment of biomarker response (IBR) showed that there were dose-dependent and time-dependent effects of Cd²⁺ exposure on Schizopygopsis younghusbandi larvae. Schizopygopsis younghusbandi larvae were sensitive to Cd²⁺, which caused adverse effects at a concentration as low as 2.5 μg/L. In summary, the results indicated that Cd²⁺ causes thyroid disruption and developmental toxicity in Schizopygopsis younghusbandi larvae and that wild Schizopygopsis younghusbandi larvae living in the Lhasa River are at potential ecological risk.

Keywords: Cd(2+); Developmental toxicity; Ecological risk; Schizopygopsis younghusbandi; Thyroid disruption.