PUBLICATION
BDE-47 induced apoptosis in zebrafish embryos through mitochondrial ROS-mediated JNK signaling
- Authors
- Zhuang, J., Pan, Z.J., Mengqiu-Li, ., Hong, F.S., Zhu, C.K., Wu, N., Chang, G., Wang, H., Zhao, X.X.
- ID
- ZDB-PUB-201002-96
- Date
- 2020
- Source
- Chemosphere 258: 127385 (Journal)
- Registered Authors
- Keywords
- Developmental toxicity, Molecular mechanism, Polybrominated diphenyl ethers, Zebrafish
- MeSH Terms
-
- Animals
- Antioxidants/metabolism
- Apoptosis/drug effects
- Embryo, Nonmammalian/drug effects
- Embryonic Development/drug effects
- Halogenated Diphenyl Ethers/toxicity*
- MAP Kinase Signaling System
- Mitochondria/metabolism
- Oxidative Stress/drug effects
- Reactive Oxygen Species/metabolism
- Water Pollutants, Chemical/toxicity*
- Zebrafish/metabolism
- PubMed
- 32947675 Full text @ Chemosphere
Citation
Zhuang, J., Pan, Z.J., Mengqiu-Li, ., Hong, F.S., Zhu, C.K., Wu, N., Chang, G., Wang, H., Zhao, X.X. (2020) BDE-47 induced apoptosis in zebrafish embryos through mitochondrial ROS-mediated JNK signaling. Chemosphere. 258:127385.
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping