Effects of PM2.5 sub-chronic exposure on liver metabolomics in mice
- VernacularTitle:PM2.5亚慢性暴露对小鼠肝脏代谢组学的影响
- Author:
Liu YANG
1
;
Siqi DOU
1
;
Xinyuan LI
1
;
Shuo WEN
1
;
Kun PAN
2
;
Biao WU
2
;
Jinzhuo ZHAO
2
;
Jianjun XU
3
;
Peng LYU
1
Author Information
- Publication Type:Experiment
- Keywords: fine particulate matter; liver; metabolomics; liquid chromatography-mass spectrometry
- From: Journal of Environmental and Occupational Medicine 2024;41(2):207-213
- CountryChina
- Language:Chinese
- Abstract: Background Atmospheric fine particulate matter (PM2.5) can disrupt the metabolic homeostasis of the liver and accelerate the progression of liver diseases, but there are few studies on the effects of sub-chronic PM2.5 exposure on the liver metabolome. Objectives To investigate the effects of sub-chronic exposure to concentrated PM2.5 on hepatic metabolomics in mice by liquid chromatography-mass spectrometry (LC-MS), and to identify potentially affected metabolites and metabolic pathways. Methods Twelve male C57BL/6J (6 weeks old) mice were randomly divided into two groups: a concentrated PM2.5 exposure group and a clean air exposure group. The mice were exposed to concentrated PM2.5 using the "Shanghai Meteorological and Environmental Animal Exposure System" at Fudan University. The exposure duration was 8 h per day, 6 d per week, for a total of 8 weeks. The mice's liver tissues were collected 24 h after the completion of exposure. LC-MS was performed to assess changes in the hepatic metabolome. Orthogonal partial least squares discriminant analysis and t-test were employed to identify differentially regulated metabolites between the two groups under the conditions of variable important in projection (VIP)≥1.0 and P<0.05. Metabolic pathway enrichment analysis was performed using MetaboAnalyst 5.0 software and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Results A total of 297 differentially regulated metabolites were identified between the concentrated PM2.5 exposure group and the clean air group. Among these metabolites, 142 were upregulated and 155 were downregulated. A total of 38 metabolic pathways were altered, with 7 pathways showing significant perturbation (P<0.05). These pathways involved amino acid metabolism, glucose metabolism, nucleotide metabolism, as well as cofactor and vitamin metabolism. The 7 significant metabolic pathways were pantothenic acid and coenzyme A biosynthesis; purine metabolism; amino sugar and nucleotide sugar metabolism; arginine biosynthesis; alanine, aspartate and glutamate metabolism; aminoacyl-tRNA biosynthesis; and fructose and mannose metabolism. Conclusion The results from metabolomics analysis suggest that sub-chronic exposure to PM2.5 may disrupt hepatic energy metabolism and induce oxidative stress damage. Aspartic acid, succinic acid, ornithine, fumaric acid, as well as purine and xanthine derivatives, were identified as potential early biomarkers of hepatic response to sub-chronic PM2.5 exposure.
