Disturbance of Brain Metabolites in Mice: Potential Neuropathic Damage Mediated by Nanocarbon Black Exposure

This Carbon black nanoparticles (CBNPs), a common and important manufacturing material, have been proven to exert adverse effects on brain function; however, the underlying neurotoxicity remains poorly understood. To unravel the deteriorating effect of CBNPs on the brain, a chronic long-term carbon black exposure mouse model (0 , 0.15 mg/ml, 0.5 mg/ml, 1.5 mg/ml groups) was established via nasal injection of CBNPs for 3 months. Intriguingly, the evidence directly showed the penetration of CBNPs in the brain, as the electron microscopic data showed an obvious deposition of CBNPs in various brain regions, where the mitochondrion displayed significant destruction. The metabolite changes based on GC/MS metabolic analysis displayed striking differences after CBNP exposure. With principal component analysis and the PLS-DA model, the brain metabolites of the control group and the treatment group were significantly distinguished, and these changes were involved in phenylalanine, tyrosine and tryptophan biosynthesis, D -glutamine and D-glutamate metabolism and linoleic acid metabolism. In detail, glutamine, glycine, lactic acid and norepinephrine, the excitotoxic metabolites, were markedly increased. Collectively, the current study provides new insights into brain metabolic homeostasis after CBNP exposure, revealing potential targets in CBNP-induced neurotoxicity.