2. Academic Validation
  3. BDE-47 induced apoptosis in zebrafish embryos through mitochondrial ROS-mediated JNK signaling

BDE-47 induced apoptosis in zebrafish embryos through mitochondrial ROS-mediated JNK signaling

  • Chemosphere. 2020 Nov;258:127385. doi: 10.1016/j.chemosphere.2020.127385.
Juan Zhuang 1,  Zheng-Jun Pan 2,  Mengqiu-Li 3,  Fa-Shui Hong 2,  Chuan-Kun Zhu 2,  Nan Wu 2,  Guoliang Chang 2,  Hui Wang 2,  Xiang-Xiang Zhao 4
Affiliations

Affiliations

  • 1 Jiangsu Key Laboratory for Eco-Agricultural Biotechnology Around Hongze Lake, School of Life Science, Huaiyin Normal University, Huai'an, China; Jiangsu Collaborative Innovation Center of Regional Modern Agriculture & Environmental Protection, Huaiyin Normal University, Huai'an, China. Electronic address: zhuangjuan1977@163.com.
  • 2 Jiangsu Key Laboratory for Eco-Agricultural Biotechnology Around Hongze Lake, School of Life Science, Huaiyin Normal University, Huai'an, China; Jiangsu Collaborative Innovation Center of Regional Modern Agriculture & Environmental Protection, Huaiyin Normal University, Huai'an, China.
  • 3 Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China.
  • 4 Jiangsu Key Laboratory for Eco-Agricultural Biotechnology Around Hongze Lake, School of Life Science, Huaiyin Normal University, Huai'an, China; Jiangsu Collaborative Innovation Center of Regional Modern Agriculture & Environmental Protection, Huaiyin Normal University, Huai'an, China. Electronic address: xxzhao2013@163.com.
PMID: 32947675 DOI: 10.1016/j.chemosphere.2020.127385
Abstract

2,2,4,4-tetrabromodiphenyl ether (BDE-47) has received considerable attention because of its high detection level in biological samples and potential developmental toxicity. Here, using zebrafish (Danio rerio) as the experimental animal, we investigated developmental effects of BDE-47 and explored the potential mechanism. Zebrafish embryos at 4 h post-fertilization (hpf) were exposed to 0.312, 0.625 and 1.25 mg/L BDE-47 to 74-120 hpf. We found that BDE-47 instigated a dose-related developmental toxicity, evidenced by reduced embryonic survival and hatching rate, shortened body length and increased aberration rate. Meanwhile, higher doses of BDE-47 reduced mitochondrial membrane potential and ATP production but increased Apoptosis in zebrafish embryos. Expression of genes involved in mitochondrial Oxidative Phosphorylation (OXPHOS) (ndufb8, sdha, uqcrc1, cox5ab and atp5fal) were negatively related to BDE-47 doses in zebrafish embryos. Moreover, exposure to BDE-47 at 0.625 or 1.25 mg/L impaired mitochondrial biogenesis and mitochondrial dynamics. Our data further showed that BDE- 47 exposure induced excessive Reactive Oxygen Species (ROS) and oxidative stress, which was accompanied by the activation of c-Jun N-terminal Kinase (JNK). Antioxidant NAC and JNK inhibition could mitigate Apoptosis in embryos and improve embryonic development in BDE-47-treated zebrafish, suggesting the involvement of ROS/JNK pathway in embryonic developmental changes induced by BDE-47. Altogether, our data suggest here that developmental toxicity of BDE-47 may be associated with mitochondrial ROS-mediated JNK signaling in zebrafish embryo.

Keywords

Developmental toxicity; Molecular mechanism; Polybrominated diphenyl ethers; Zebrafish.

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