Long-Term Exposure to Neonicotinoid Insecticide Acetamiprid at Environmentally Relevant Concentrations Impairs Endocrine Functions in Zebrafish: Bioaccumulation, Feminization, and Transgenerational Effects

Neonicotinoid insecticides have attracted worldwide attention due to their ubiquitous occurrence and detrimental effects on aquatic organisms, yet their impacts on fish reproduction during long-term exposure remain unknown. Here, zebrafish (F0) were exposed to a neonicotinoid, acetamiprid, at 0.19-1637 mu g/L for 154 d. Accumulation and biotransformation of acetamiprid were observed in adult fish, and the parent compound and its metabolite (acetamiprid-N-desmethyl) were transferred to their offspring. Acetamiprid caused slight survival reduction and significant feminization in F0 fish even at the lowest concentration. Hormone levels in F0 fish were remarkedly altered, that is, gonad 17 beta-estradiol (E2) significantly increased, while androstenedione decreased. The corresponding transcription of steroidogenic genes (ar, cyp19b, fsh beta, gnrh2, gnrh3, and lh beta) were significantly upregulated in the brain and gonad of the females but downregulated in the males. The vtg1 gene expression in the liver of male fish was also upregulated. In addition to F0 fish, parental exposure to acetamiprid decreased hatchability and enhanced malformation of F1 embryos. Chronic exposure to acetamiprid at environmentally relevant concentrations altered hormone production and the related gene expression of the hypothalamic-pituitary-gonad (HPG) axis in a sex-dependent way, caused feminization and reproductive dysfunction in zebrafish, and impaired production and development of their offspring.

Automated summary

This study found that long-term exposure to acetamiprid may cause feminization and reproductive dysfunction in zebrafish, as well as impair the production and development of their offspring. Acetamiprid also affected hormone production and the transcription levels of related genes in fish.