ORIGINAL RESEARCH
Disturbance of Brain Metabolites in Mice:
Potential Neuropathic Damage Mediated
by Nanocarbon Black Exposure
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1
Key Laboratory of Modern Toxicology (NJMU), Ministry of Education; Department of Toxicology,
School of Public Health, Nanjing Medical University, 211166, China
2
Department of Emergency Medicine, the First Affiliated Hospital of Nanjing Medical University, 210029, China
3
School of Food Science, State Key Laboratory of Food Science and Technology, Jiangnan University, 214122, China
4
Department of Physical and Chemical Inspection,the Affiliated Wuxi Center for Disease Control
and Prevention of Nanjing Medical University, 211166, China
These authors had equal contribution to this work
Submission date: 2023-07-22
Final revision date: 2023-08-29
Acceptance date: 2023-09-21
Online publication date: 2024-01-12
Publication date: 2024-02-28
Corresponding author
Wenwei Liu
Department of Physical and Chemical Inspection,the Affiliated Wuxi Center for Disease Control
and Prevention of Nanjing Medical University,211166, China
Pol. J. Environ. Stud. 2024;33(3):2103-2112
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ABSTRACT
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.