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Effects of concentrated ambient fine particles on plasma glycerophosphocholine in a myocardial rat model
particulate matter,cardiovascular disease,lipidomics,phosphatidylcholine (PC),nuclear magnetic resonance (NMR),mass spectrometry (MS),
|Publication Year :||2010|
Many epidemiologic studies have demonstrated that fine particles (PM2.5) will produce cardiovascular adverse effects, especially for those who already have cardiovascular disease. There have been two hypotheses about the mechanisms of ambient particulate in cardiovascular system. The first one is through direct effect. PM or its’ soluble materials activate the neural reflexes and disarray the heart rate rhythm, which sequentially conducting the cardiac arrhythmias. The other one is the indirect effect, which caused by increased oxidative stress and inflammation, then inducing the thrombosis and the atherosclerosis. Either direct effects or indirect effects will disturb the lipids’ balance during the course of cardiovascular disease. Glycerophosphocholine (PC), which accounted the most ratios in phospholipids, are likely to be affected by PM2.5 exposure and cause cardiovascular abnormal. In our study, we compare the differences of PC in myocardial rat plasma between PM2.5 exposure and control group. We intend to examine the molecular events of concentrated ambient particles in plasma of susceptible population.
Male SD rats were exposed to PM2.5 for 65 days after they became myocardial damaging rats by isoproterenol(150 mg/kg). After animals were scarified, plasma samples were taken and snap frozen. The samples were extracted by Folch’s extraction method and the hydrophobic layer was removed for farther analysis. Both NMR and MS were used to analyze the hydrophobic metabolite extracts of the rat plasma. The data from NMR and MS were pretreated for multivariate analysis to examine the hydrophobic metabolic variation among samples.
The statistic results demonstrated lipid fluctuations in rat plasma after PM2.5 exposure. NMR data showed that fatty acyl chain -CH2CH= and =CHCH2CH= decreased in exposure group. The raised oxidative stress after PM2.5 exposure may explain the decline of unstaurated fatty acyl chain. MS data indicated that the concentrations of lysoPCs were declined in exposure group. Moreover, numerous diacyl-phosphatidylcholine and alkyl-acyl-phosphatidylcholine were increased in the plasma of PM2.5 exposed rats.
Understanding the fluctuations of PC in plasma can help us to elucidate the possible mechanism of PM2.5 toxicity and to mine the possible biomarkers for cardiovascular disease progress.
|Appears in Collections:||環境衛生研究所|
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