| 作者： |
Yang, Lihua; Zhu, Biran; Zhou, Shanqi; Zhao, Min; Li, Ruiwen; Zhou, Yuxi; Shi, Xiongjie; Han, Jian; Zhang, Wei; Zhou, Bingsheng |
| 论文摘要： |
Decabromodiphenyl ethane (DBDPE),a novel brominated flame retardant,is becoming increasingly prevalent in environmental and biota samples.While DBDPE has been shown to cause various biological adverse effects,the molecular mechanism behind these effects is still unclear. Inthis research, zebrafish embryos were exposed to DBDPE (50-400 & mu;g/L) until 120 h post fertilization (hpf). The results confirmedthe neurotoxicity by increased average swimming speed, interferedneurotransmitter contents, and transcription of neurodevelopment-relatedgenes in zebrafish larvae. Metabolomics analysis revealed changesof metabolites primarily involved in glycolipid metabolism, oxidativephosphorylation, and oxidative stress, which were validated throughthe alterations of multiple biomarkers at various levels. We furtherevaluated the mitochondrial performance upon DBDPE exposure and foundinhibited mitochondrial oxidative respiration accompanied by decreasedmitochondrial respiratory chain complex activities, mitochondrialmembrane potential, and ATP contents. However, addition of nicotinamideriboside could effectively restore DBDPE-induced mitochondrial impairmentsand resultant neurotoxicity, oxidative stress as well as glycolipidmetabolism in zebrafish larvae. Taken together, our data suggest thatmitochondrial dysfunction was involved in DBDPE-induced toxicity,providing novel insight into the toxic mechanisms of DBDPE as wellas other emerging pollutants. Decabromodiphenylethane-induced glucolipid metabolism disordersand neurotoxicity in zebrafish larvae, which can be restored followingmitochondrial function recovery. |
