Cyhalofop-butyl has the potential to induce developmental toxicity, oxidative stress and apoptosis in early life stage of zebrafish (Danio rerio)
Cyhalofop-butyl is a selective herbicide widely employed in paddy field, which can transfer into aquatic environments. However, details of the environmental risk and aquatic toxicity of cyhalofop-butyl have not been fully investigated. In this study, zebrafish (Danio rerio) embryos were exposed to a...
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Veröffentlicht in: | Environmental pollution (1987) 2015-08, Vol.203, p.40-49 |
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Sprache: | eng |
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Zusammenfassung: | Cyhalofop-butyl is a selective herbicide widely employed in paddy field, which can transfer into aquatic environments. However, details of the environmental risk and aquatic toxicity of cyhalofop-butyl have not been fully investigated. In this study, zebrafish (Danio rerio) embryos were exposed to a range of cyhalofop-butyl until 120 hour post-fertilization (hpf) to assess embryonic toxicity of the chemical. Our results demonstrated that cyhalofop-butyl was highly toxic to zebrafish embryos, with concentration-dependent negative effects in embryonic development. In addition, exposure to cyhalofop-butyl resulted in significant increases in reactive oxygen species (ROS) production and cell apoptosis in heart area. The mRNA levels of the genes related to oxidative stress and apoptosis were also altered significantly after cyhalofop-butyl exposure. Moreover, the activity of capspase-9 and caspase-3 were significantly increased. Therefore, we speculated that oxidative stress-induced apoptosis should be responsible for abnormal development during embryogenesis after cyhalofop-butyl exposure.
•Cyhalofop-butyl can induce developmental toxicity in zebrafish embryos.•Cyhalofop-butyl can induce oxidative stress and apoptosis in zebrafish embryos.•Oxidative stress-induced apoptosis might be responsible for abnormal development.
Cyhalofop-butyl could induce negative effects in embryonic development. The cyhalofop-butyl – induced developmental toxicity could be explained by oxidative stress-induced apoptosis. |
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ISSN: | 0269-7491 1873-6424 |
DOI: | 10.1016/j.envpol.2015.03.044 |