Alterations in rat pulmonary phosphatidylcholines after chronic exposure to ambient fine particulate matter

Abstract

This study elucidated the underlying pathophysiological changes that occur after chronic ambient fine particulate matter (PM2.5) exposure via a lipidomic approach. Five male Sprague-Dawley rats were continually whole-body exposed to ambient air containing PM2.5 at 16.7 ± 10.1 μg m(-3) from the outside of the building for 8 months, whereas a control group (n = 5) inhaled filtered air. Phosphorylcholine-containing lipids were extracted from lung tissue and profiled using ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The phosphatidylcholine (PC) signal features of the two groups were compared using partial least squares discriminant analysis (PLS-DA) and Wilcoxon rank sum tests. The PC profile of the exposure group differed from that of the control group; the R(2)Y and Q(2) were 0.953 and 0.677, respectively, in the PLS-DA model. In the exposure group, a significant 0.66- to 0.80-fold reduction in lyso-PC levels, which may have resulted from repeated inflammation, was observed. Decreased surfactant PCs by 16% at most may indicate injuries to alveolar type II cells. Cell function and cell signalling are likely to be altered because the decrease in unsaturated PCs may reduce membrane fluidity. Accompanied by the decline in plasmenylcholines, decreased unsaturated PCs may indicate the attack of reactive oxygen species generated by PM2.5 exposure. The physiological findings conformed to the histopathological changes in the exposed animals. PC profiling using UPLC-MS/MS-based lipidomics is sensitive for reflecting pathophysiological perturbations in the lung after long-term and low concentration PM2.5 exposure.

Mass spectrometry-based lipidomics to explore the biochemical effects of naphthalene toxicity or tolerance in a mouse model

“…The decreasing level of three P-PCs, including PC(P-16:0/16:0), PC(P-16:1/20:3), and PC(P-38:5) in the tolerant group compared with the control group may imply that the consumption of sacrificial oxidants or scavengers against the naphthalene induced molecular perturbations to protect other membrane components. A similar reduction trend of P-PCs was also observed in the lungs of rats chronically exposed to ambient fine particulate matter [ 21 ]. In our previous study [ 14 ], an significant increase in acetone in the bronchoalveolar lavage fluid (BALF) from the same injured mice was found.…”

“…SMs not only play an important role in the membrane microenvironments (such as caveolae and lipid rafts) [ 18 ] but also in the precursor pool of second messengers for cellular signal transduction [ 19 ]. Previously, our laboratory developed a validated liquid chromatography-tandem MS platform to monitor the alterations of different phosphorylcholine-containing lipids and apply them in studying pulmonary toxicity [ 20 , 21 ].…”

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

“…However, another study found that PM 2.5 decreased the levels of these metabolites in pulmonary tissue [17]. In that study, PM 2.5 was given to rats through ambient air for 8 months and histopathology revealed emphysema [17]; however, in our study, PM 2.5 was given to rats through acute instillation, and histopathology only exhibited edema and infiltration of PMNs in the alveolar septum, which is a different stage of PM 2.5 -induced pulmonary injury. In the early stage of pulmonary injury, the elevation of LPC and PC levels was a response to PM 2.5 stimulation.…”

“…The imbalance of Cer and S1P leads to alveolar enlargement or fibrosis and is involved in the onset of COPD, asthma, lung fibrosis and lung cancer [16]. Although a phospholipid metabolism profile of pulmonary tissue after PM 2.5 exposure has been carried out [17], the global lipid metabolism change induced by PM 2.5 is largely unknown.…”

Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)

“…It has also been suggested that vascular endothelial growth factor receptor (VEGF), mitogen-activated protein kinase (MAPK), nuclear factor κB (NF-κB) and interleukin (IL)-8 signaling is involved in PM2.5-induced lung injury (8). In PM2.5-exposed rats, a decrease in phosphatidylcholine levels may be detected, which may impair alveolar type II cells and alter cell functions (9). In addition, PM2.5 exposure has been demonstrated to be associated with endothelial cell…”