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Fluxapyroxad disrupt erythropoiesis in zebrafish (Danio rerio) embryos
Xin Chen1, Tiantong Qiu1, Mengjun Pan1
1Engineering Research Center of Molecular Medicine of Ministry of Education, Key Laboratory of Fujian Molecular Medicine, Key Laboratory of Xiamen Marine and Gene Drugs, Key Laboratory of Precision Medicine and Molecular Diagnosis of Fujian Universities, School of Biomedical Sciences, Huaqiao University, Xiamen 361021, PR China.
Abstract:
Fluxapyroxad, a succinate dehydrogenase inhibitor (SDHI) fungicide, is commercialized worldwide to control a variety of fungal diseases. Growing evidence shows that fluxapyroxad is teratogenic to aquatic organisms. In this study, the influence of fluxapyroxad toward hematopoietic development was evaluated using zebrafish embryos which were exposed to fluxapyroxad (0.03 µM, 0.3 µM and 3 µM) from 3 h post fertilization (hpf) to 3 days post fertilization (dpf). Compared to the control groups, the hemoglobin was ectopic and decreased in response to fluxapyroxad treatment. The transcription levels of genes (hbbe1, hbbe2, and gata1a) involved in erythropoiesis were reduced after exposure to fluxapyroxad. In contrast, the distributions and expression of marker genes for myeloid lineage cells were unaffected by fluxapyroxad exposure. Our data suggested that fluxapyroxad might specifically affect erythropoiesis and hold great promise for the assessment of the toxicity of fluxapyroxad to aquatic organisms.
Insights
Fluxapyroxad fungicide exposure disrupts red blood cell development in zebrafish embryos. This study reveals specific impacts on erythropoiesis, highlighting potential risks to aquatic organisms from this common pesticide.
Area of Science:
- Environmental Toxicology
- Developmental Biology
- Ecotoxicology
Background:
- Fluxapyroxad, a widely used succinate dehydrogenase inhibitor (SDHI) fungicide, is known to exhibit teratogenic effects on aquatic life.
- Understanding the specific mechanisms of fluxapyroxad toxicity is crucial for assessing its environmental impact.
Purpose of the Study:
- To investigate the effects of fluxapyroxad exposure on hematopoietic development in zebrafish embryos.
- To determine if fluxapyroxad specifically targets erythropoiesis or affects other hematopoietic lineages.
Main Methods:
- Zebrafish embryos were exposed to varying concentrations of fluxapyroxad (0.03 µM, 0.3 µM, 3 µM) from 3 hours post-fertilization (hpf) to 3 days post-fertilization (dpf).
- Hematopoietic development was assessed by examining hemoglobin levels and the expression of key erythropoiesis-related genes (hbbe1, hbbe2, gata1a).
- The distribution and expression of myeloid lineage marker genes were also analyzed.
Main Results:
- Fluxapyroxad exposure led to decreased and ectopic hemoglobin distribution in zebrafish embryos compared to control groups.
- Significant reductions in the transcription levels of erythropoiesis genes (hbbe1, hbbe2, gata1a) were observed following fluxapyroxad treatment.
- Myeloid lineage cell development and gene expression remained unaffected by fluxapyroxad exposure, indicating a specific impact on red blood cell formation.
Conclusions:
- Fluxapyroxad specifically inhibits erythropoiesis in zebrafish embryos, suggesting a targeted mechanism of toxicity.
- These findings provide valuable insights into the ecotoxicological risks of fluxapyroxad to aquatic organisms, particularly concerning blood development.
- The study supports the use of zebrafish embryos as a model for assessing the developmental toxicity of fluxapyroxad and similar fungicides.
