Xue Ma

Agricultural use of neonicotinoid insecticides is increasing worldwide, posing a risk to nontarget organisms. The present study investigated developmental toxicity of a widely used neonicotinoid, acetamiprid, to zebrafish embryos. Sublethal (malformations, hatchability, heart rate, body length, alteration of spontaneous movement and touch responses) and lethal effects were monitored during exposure period from 6 h post fertilization (hpf) to 120 hpf. Zebrafish embryos exhibited significant mortality and teratogenic effects at acetamiprid concentration greater than 263 mg/L, with bent spine being the main malformation. Toxicity spectra were constructed to rank the sensitivity of individual end points to acetamiprid exposure and impaired spontaneous movement was the most sensitive end point of those tested. The present study provides the basis for understanding developmental toxicity of acetamiprid exposure to zebrafish embryos. This information is critical for future studies evaluating aquatic risk from neonicotinoids as little is known regarding adverse effects of neonicotinoids to aquatic vertebrate species.

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.