Exposure to Boscalid Induces Reproductive Toxicity of Zebrafish by Gender-Specific Alterations in Steroidogenesis.

Boscalid is a succinate dehydrogenase inhibitor fungicide and is frequently detected in surface water. Due to the frequent detection of boscalid, we evaluated its impact on the reproduction of adult zebrafish following a 21 d exposure to 0, 0.01, 0.1, and 1.0 mg/L. Following exposure to boscalid, the fertility of female zebrafish and fertilization rate of spawning eggs were reduced in a concentration-dependent manner up to a respective 87% and 20% in the highest concentration. A significant 16% reduction in the percentage of late vitellogenic oocytes was noted in ovaries, and a significant 74% reduction in the percentage of spermatids in testis was also observed after treatment with 1.0 mg/L. 17β-Estradiol (E2) concentrations decreased significantly in females (34% decrease) but significantly increased in males (15% increase) following 1.0 mg/L boscalid treatment. The expression of genes (such as , , , and ) related to the hypothalamus-pituitary-gonad-liver (HPGL) axis was significantly altered and positively correlated with E2 concentrations in female and male zebrafish ( < 0.05). Molecular docking results revealed that the binding modes between boscalid and target proteins (ER and CYP19) of zebrafish were similar to that of the reference compounds and the target proteins. The binding energies indicate that boscalid may have a weak estrogen-like binding effect or CYP19 inhibition, potentially altering the HPGL axis, thereby reducing E2 concentrations and fecundity in females. In contrast, boscalid caused significant induction of E2 steroidogenesis and subsequent feminization of gonads in males, indicating gender-specific adverse outcome pathways.