Metabolomic insights into the lasting impacts of early-life exposure to BDE-47 in mice.
Early-life exposure to toxicants may have lasting effects that adversely impact later development. Thus, although the production and use of a toxicant have been banned, the risk to previously exposed individuals may continue. BDE-47, a component of commercial penta-BDEs, is a persistent organic pollutant with demonstrated neurotoxicity. To investigate the persistent effects of BDE-47 and the mechanisms thereof, we employed a metabolomics approach to analyze the brain, blood and urine of mice exposed to BDE-47 for 28 days and then 3 months post-exposure. In the brain, BDE-47 was detectable just after exposure but was below the limit of detection (LOD) 3 months later. However, the metabolomic alterations caused by early-life exposure to BDE-47 persisted. Potential biomarkers related to these alterations included phosphatidylcholine, lysophosphatidylcholine, sphingomyelin and several amino acids and biogenic amines. The metabolic pathways involved in the response to BDE-47 in the brain were mainly those related to glycerophospholipid metabolism, sphingomyelin metabolism and neurotransmitter regulation. Thus, our study demonstrates the utility of metabolomics, as the omics most closely reflecting the phenotype, in exploring the mechanisms underlying the lasting effects induced by early-life BDE-47 exposure.