AI Article Synopsis
- Amisulbrom, an oomycete-specific fungicide, negatively affects zebrafish embryo development, impairing the visual phototransduction system.
- Exposure to amisulbrom led to issues like microphthalmia, altered gene expression related to retinal cell differentiation, and increased retinal cell death.
- The study highlights amisulbrom's toxicity to eye development, raising concerns about its ecological impact on aquatic life.
Article Abstract
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 μM 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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| http://dx.doi.org/10.1007/s11356-023-25584-7 | DOI Listing |
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