Fine particulate matter (PM2.5) exposure alters brain development, clinical cognition and behavior in childhood. Previous studies of this subject have mainly been epidemiological investigations or analyses of gene and protein levels; however, gas chromatography-mass spectrometry (GC-MS)-based metabolic profiling, which will help clarify the molecular mechanisms of susceptibility in PM2.5-induced neurotoxicity, is lacking. In the present study, C57BL/6 mice at different ages (4 weeks, 4 months and 10 months) received oropharyngeal aspiration of PM2.5 (3 mg/kg) every other day for 4 weeks. The Morris water maze showed that PM2.5 exposure caused deterioration of spatial learning and memory in young (4 week old) mice. In addition, the levels of several metabolites belonging to different metabolite classes were significantly changed by PM2.5 exposure in 4-week-old mice. Based on metabolic pathway analysis, we speculated that the decline in spatial learning and memory due to PM2.5 exposure may be directly or indirectly associated with hippocampal region-specific metabolic alterations involving energy metabolism (citric acid, succinic acid, malic acid, maltose and creatinine); cholesterol metabolism (desmosterol, lanosterol and campesterol); arachidonic acid metabolism (methyl arachidonic acid, nonanoic acid and linoleic acid); inositol phosphate metabolism (myo-inositol, myo-inositol-1-phosphate and methyl-phosphate) and aspartic acid metabolism (aspartic acid, asparagine and homoserine).
Keywords: Different developmental windows; Fine particulate matter (PM(2.5)) exposure; Hippocampal metabolomics; Neurological damages.
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