Flurochloridone (FLC) is a selective herbicide that can cause reproductive toxicity in male rats. However, limited information is available regarding the toxicity of FLC in the developmental stages of aquatic organisms. This study aimed to investigate the effects of FLC exposure during embryonic development and elucidate its potential mechanism of action. Zebrafish embryos were exposed to 6.25, 12.5, 25, and 50 μg/mL FLC for 4–144 hpf. The developmental status of embryos was recorded; the indicators of oxidative stress and embryonic apoptosis were determined. We found that FLC exposure caused severe embryonic malformations, such as pericardial edema, spinal curvature, and growth retardation, accompanied by a decreased hatching and survival rate. After exposure until 144 h postfertilization, the median lethal concentration (LC50) of FLC in zebrafish embryos was 36.9 μg/mL. Subsequently, FLC induced the accumulation of reactive oxygen species and malondialdehyde, enhanced the activity of superoxide dismutase, and activated the Keap1–Nrf2 signaling pathway. Further studies confirmed that FLC can induce apoptosis in zebrafish embryos through the activation of caspase. These results suggest that FLC induced developmental toxicity in zebrafish embryos, which provides new evidence regarding FLC toxicity in aquatic organisms and to assess human health risks.

中文翻译：

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氟氯酮对斑马鱼 （Danio rerio） 胚胎发育毒性的影响


氟氯酮 （FLC） 是一种选择性除草剂，可对雄性大鼠造成生殖毒性。然而，关于 FLC 在水生生物发育阶段的毒性的信息有限。本研究旨在探讨胚胎发育过程中 FLC 暴露的影响，并阐明其潜在的作用机制。斑马鱼胚胎暴露于 6.25、12.5、25 和 50 μg/mL FLC 中 4-144 hpf。记录胚胎的发育状态;测定氧化应激和胚胎凋亡指标。我们发现 FLC 暴露导致严重的胚胎畸形，如心包水肿、脊柱弯曲和生长迟缓，并伴有孵化率和存活率降低。暴露后至受精后 144 小时，斑马鱼胚胎中 FLC 的中位致死浓度 （LC50） 为 36.9 μg/mL。随后，FLC 诱导活性氧和丙二醛的积累，增强超氧化物歧化酶的活性，并激活 Keap1-Nrf2 信号通路。进一步研究证实，FLC 可通过激活 caspase 诱导斑马鱼胚胎凋亡。这些结果表明，FLC 诱导斑马鱼胚胎的发育毒性，这为 FLC 在水生生物中的毒性和评估人类健康风险提供了新证据。