https://doi.org/10.1016/j.jhazmat.2025.140693. Journal of Hazardous Materials，2025

Abstract

Imidacloprid (IMI) poses risks to aquatic ecosystems and exhibits visual toxicity to nontarget organisms. However, the underlying mechanism of its visual toxicity has not been fully elucidated. After exposure to IMI at the concentrations 10, 100, and 1000 µg/L for 4 or 21 days, the visual behavior of zebrafish larvae was first suppressed, followed by enhanced locomotor and visual activities as exposure prolonged. The eye development in zebrafish larvae was significantly disrupted.

Structurally, the lens area of zebrafish larvae was reduced from 15.63 % to 50.21 % (4 days) and from 37.00 % to 47.22 % (21 days), and the retina exhibited a thickening of the OPL and IPL, along with thinning of the RPE. Genes related to lens structure (e.g., CRYBA4 and CRYBB2) were significantly down-regulated at 4 days (100 and 1000 µg/L) and then up-regulated (10 and 100 µg/L) at 21 days at the mRNA and protein levels (P < 0.05). Furthermore, IMI exposure disrupted the phototransduction and retinol metabolism cascade in zebrafish larvae, which involves the generation of visual signals across three critical stages, namely, light input, photopigment activation, and photoelectric conversion. Generally, the key genes and metabolites associated with these processes (e.g., Rhodopsin, OPN1SW1, GNGT1, REP65A, 11-cis-retinal) were significantly decreased in zebrafish exposed to IMI for 4 days and increased in those exposed for 21 days (P < 0.05). Therefore, the abnormal color perception was observed in exposed zebrafish larvae. This study elucidates the mechanism underlying IMI-induced visual toxicity in zebrafish and provides crucial theoretical insights for assessing the visual toxicity of agrochemicals.

Graphical Abstract

Journal of Hazardous Materials，IF=11.3

https://doi.org/10.1016/j.jhazmat.2025.140693