Nicotinamide Riboside Protects Against Neurotoxicity in Zebrafish: Preclinical Findings

Synopsis

Decabromodiphenyl ethane (DBDPE) is a new flame retardant that is increasingly found in the environment and living organisms. Its harmful effects on biology are known, but the exact mechanisms were unclear. In this study, zebrafish embryos were exposed to DBDPE, which caused neurotoxicity, including faster swimming, disrupted neurotransmitter levels, and changes in genes important for brain development. Metabolomics showed that DBDPE affected energy use, fat and sugar metabolism, and caused oxidative stress. Mitochondria—the cell’s energy factories—were damaged, showing lower respiration, reduced ATP, and weaker membrane potential. Treatment with nicotinamide riboside (NR) helped restore mitochondrial function, reduced oxidative stress, normalized metabolism, and improved neurotoxicity. These results suggest that mitochondrial dysfunction drives DBDPE toxicity and highlight potential strategies, like NR supplementation, to counteract its harmful effects.

Journal

Environmental Science & Technology