Thyroid Hormone Disruption and Developmental Toxicity of Diuron and Irgarol 1051 in Zebrafish (Danio rerio) Larvae

Antifouling biocides are marine pollutants intentionally used on vessels and are frequently detected in aquatic environments. The effects of Diuron and Irgarol 1051 (Irgarol), persistent antifouling biocides in the marine environment, on various aquatic organisms remain incompletely understood. In this study, we investigated whether Diuron and Irgarol disrupt thyroid hormone function in fish, using zebrafish larvae as a model. Both compounds induced reductions in survival and hatching rates. Notably, Diuron caused edema and posterior swim bladder noninflation even at a concentration as low as 0.6 mg/L. According to the adverse outcome pathway (AOP) published by the Organisation for Economic Co-operation and Development for thyroid hormone disruption, posterior swim bladder noninflation is one of the adverse outcomes. Based on this, we examined changes in the expression of thyroid-related genes. Diuron exposure significantly decreased dio1 and tshb expression, while significantly increasing thrb expression. Dio1 is an enzyme responsible for converting T4 to T3, and its inhibition is identified as a key event in the published AOP. In contrast, Irgarol exposure significantly increased thrb expression but did not cause significant changes in other thyroid-related genes. These findings suggest that both Diuron and Irgarol affect embryonic development and hatching in zebrafish and that Diuron has the potential to disrupt thyroid hormone function.