Identification of multiple dysregulated metabolic pathways by GC-MS-based profiling of liver tissue in mice with OVA-induced asthma exposed to PM2.5

Abstract

Particulate matter (PM) exposure increases the risk of asthma. However, the effect of PM2.5 exposure on liver metabolism in mice with asthma symptoms remains unclear. We established an ovalbumin (OVA)-induced asthma model in mice and divided the animals into four groups: control group (C), PM2.5 exposure group (P), OVA-induced asthma group (O) and OVA-induced asthma PM2.5 exposure group (OP). Gas chromatography-mass spectrometry (GC-MS) was used to identify the metabolite markers and related perturbed metabolic pathways in mouse liver tissue after PM2.5 exposure. Multivariate analysis showed 9 and 12 potential metabolite markers in the P and OP groups, respectively, after PM2.5 exposure that were significantly correlated with lipid peroxidation indices. PM2.5 exposure perturbed 5 and 7 metabolic pathways in the P and OP groups, respectively. These metabolic pathways mainly involve the lipid metabolism, amino acid metabolism, carbohydrate metabolism, and nucleotide metabolism. These results highlight the potential to study PM2.5-triggered alterations via liver tissue in normal and OVA-induced asthmatic mice to gain a more realistic appraisal of the resulting early toxicity events. Additionally, these results revealed potential metabolite markers of early antioxidant defense events triggered by PM2.5 and indicated that metabolite markers are more sensitive than antioxidant indicators.