Human exposure to fine particulate matter (PM2.5) in various environment could lead to a number of adverse health effects. Little is known about the toxic mechanism and the further response caused by PM2.5 exposure. In this study, a metabolomics approach using gas chromatography-mass spectrometry (GC-MS) was adopted to evaluate the liver toxicity induced by different gradient concentrations of PM2.5. A multivariate statistical analysis had shown, a total of 12 endogenous metabolites including amino acids and organic acids were identified as potential biomarkers of PM2.5 and most of them were down-regulated. By analyzing the metabolic pathways using the identified biomarkers, the significantly interfered metabolic pathways when mice were exposed to PM2.5 were found as: glycine, serine and threonine metabolism, aminoacyl-tRNA biosynthesis, cysteine and methionine metabolism, alanine, aspartate and glutamate metabolism, methane metabolism, linoleic acid metabolism and valine, and leucine and isoleucine biosynthesis, all of which were closely related to liver metabolism. The findings of this study reveal detailed toxic metabolic effects of PM2.5 in liver tissues, provide ways for assessing the health risk of PM2.5 at molecular level, and further offer insights on the potential mechanism of its toxicity.
Keywords: Fine particulate matter; Mechanisms of toxicity; Metabolomics.
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