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.
eISSN:2083-5906
ISSN:1230-1485
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