期刊
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
卷 30, 期 16, 页码 46248-46256出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s11356-023-25584-7
关键词
Zebrafish; Retina; Amisulbrom; Oxidative stress; Apoptosis
The purpose of this study was to evaluate the adverse effects of amisulbrom on retinal development in zebrafish. Zebrafish embryos were treated with different concentrations of amisulbrom and showed phenotypic abnormalities, dysregulation of gene transcription levels related to retinal cell layer differentiation, increased retinal apoptosis, and changes in glutathione and malondialdehyde content. These findings demonstrate the toxicity of amisulbrom to eye development and its potential ecotoxicological impacts on aquatic species.
Amisulbrom is an oomycete-specific fungicide that was developed by Nissan Chemical Industries Limited. The exposure of developing zebrafish embryo to amisulbrom caused disorders in the visual phototransduction system. However, the potential toxic mechanisms of amisulbrom on retinal development remains unclear. The research purpose of this study was to evaluate the adverse effects of amisulbrom on retinal development in a model organism, the zebrafish. Zebrafish embryos were treated with 0, 0.0075, 0.075, or 0.75 mu M amisulbrom from 3 h post-fertilization (hpf) to 72 hpf. Compared with the control group, amisulbrom-treated zebrafish embryos displayed phenotypic microphthalmia, dysregulation of gene transcription levels (alcama, prox1a, sox2, vsx1, rho, bluops, rdops, uvops, and grops) related to the retinal cell layer differentiation, and increased retinal apoptosis. In addition, the content of glutathione and malondialdehyde increased significantly after exposure to amisulbrom. Overall, our data demonstrate the toxicity of amisulbrom to eye development, which will help to assess the potential ecotoxicological impacts posed by amisulbrom to aquatic species.
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