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 μg/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 17β-estradiol (E2) significantly increased,
while androstenedione decreased. The corresponding transcription of
steroidogenic genes (ar, cyp19b, fshβ, gnrh2, gnrh3, and lhβ) 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.