Journal
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 28, Issue 27, Pages 36303-36313Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s11356-021-13238-5
Keywords
Bixafen; Fungicide; Zebrafish; Embryo; Cardiac toxicity; Apoptosis
Categories
Funding
- Young Scientists Fund of the National Natural Science Foundation of China [31801034]
- Scientific Research Funds of Huaqiao University [15BS306]
- Postgraduates' Innovative Fund in Scientific Research of Huaqiao University
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In this study, exposure to BIX was found to induce cardiac toxicity in zebrafish embryos, leading to cardiac dysplasia and dysfunction. This toxicity was associated with decreased expression of erythropoiesis-related and cardiac development-related genes in response to BIX treatment. These findings highlight the potential environmental risks of BIX exposure.
Bixafen (BIX) is a succinate dehydrogenase inhibitor (SDHI)-class fungicide that is used to control crop diseases. However, data on the toxicity of BIX to zebrafish are limited. Here, zebrafish embryos were exposed to 0.1, 0.3, and 0.9 mu M BIX. After BIX exposure, zebrafish embryos exhibited cardiac dysplasia and dysfunction, including pericardial edema, reduced heart rate, and drastically decreased erythrocytes in the cardiac area; the severity of these negative effects increased with BIX concentration and the duration of BIX exposure. In addition, the transcription levels of erythropoiesis-related genes decreased significantly in BIX-treated embryos, as compared to untreated control embryos. Similarly, compared with the control, key genes responsible for cardiac development (myh6, nkx2.5, and myh7) also exhibited dysregulated expression patterns in response to BIX treatment, suggesting that BIX might specifically affect cardiac development. Finally, cell apoptosis was induced in embryos after BIX treatment. In combination, our results suggested that exposure to BIX induced cardiac toxicity in zebrafish. These data will be valuable for future evaluations of the environmental risks of BIX.
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