Rizzo Angela Maria, Corsetto Paola Antonia, Farina Francesca, Montorfano Gigliola, Pani Giuseppe, Battaglia Cristina, Sancini Giulio, Palestini Paola
Department of Pharmacological and Biomolecular Sciences (DiSFEB), Laboratory of Membrane Biochemistry and Applied Nutrition, Università degli Studi di Milano, Milano, Italy.
Department of Health Science (DISS), POLARIS Research Center, University of Milano-Bicocca, Monza, Italy.
PLoS One. 2014 Sep 26;9(9):e106855. doi: 10.1371/journal.pone.0106855. eCollection 2014.
Adverse health effects of air pollution attributed mainly to airborne particulate matter have been well documented in the last couple of decades. Short term exposure, referring to a few hours exposure, to high ambient PM10 concentration is linked to increased hospitalization rates for cardiovascular events, typically 24 h after air pollution peaks. Particulate matter exposure is related to pulmonary and cardiovascular diseases, with increased oxidative stress and inflammatory status. Previously, we have demonstrated that repeated intratracheal instillation of PM10sum in BALB/c mice leads to respiratory tract inflammation, creating in lung a condition which could potentially evolve in a systemic toxic reaction. Additionally, plasma membrane and tissue lipids are easily affected by oxidative stress and directly correlated with inflammatory products. With this aim, in the present investigation using the same model, we analyzed the toxic potential of PM10sum exposure on lipid plasma membrane composition, lipid peroxidation and the mechanisms of cells protection in multiple organs such as lung, heart, liver and brain. Obtained results indicated that PM10 exposure led to lung lipid reshaping, in particular phospholipid and cholesterol content increases; concomitantly, the generation of oxidative stress caused lipid peroxidation. In liver we found significant changes in lipid content, mainly due to an increase of phosphatidylcholine, and in total fatty acid composition with a more pronounced level of docosahexaenoic acid; these changes were statistically correlated to lung molecular markers. Heart and brain were similarly affected; heart was significantly enriched in triglycerides in half of the PM10sum treated mice. These results demonstrated a direct involvement of PM10sum in affecting lipid metabolism and oxidative stress in peripheral tissues that might be related to the serious systemic air-pollution effects on human health.
在过去几十年中，空气污染对健康的不良影响主要归因于空气中的颗粒物，这已得到充分记录。短期暴露，即暴露几个小时于高环境PM10浓度，与心血管事件住院率增加有关，通常在空气污染峰值后24小时出现。颗粒物暴露与肺部和心血管疾病有关，会增加氧化应激和炎症状态。此前，我们已经证明，在BALB/c小鼠中反复气管内滴注PM10总和会导致呼吸道炎症，在肺部产生一种可能演变为全身毒性反应的状况。此外，质膜和组织脂质很容易受到氧化应激的影响，并与炎症产物直接相关。出于这个目的，在本研究中使用相同的模型，我们分析了暴露于PM10总和对脂质质膜组成、脂质过氧化以及肺、心、肝和脑等多个器官细胞保护机制的潜在毒性。获得的结果表明，暴露于PM10会导致肺脂质重塑，特别是磷脂和胆固醇含量增加；同时，氧化应激的产生导致脂质过氧化。在肝脏中，我们发现脂质含量有显著变化，主要是由于磷脂酰胆碱增加，以及总脂肪酸组成中二十二碳六烯酸水平更为显著；这些变化与肺分子标志物在统计学上相关。心脏和大脑也受到类似影响；在一半接受PM10总和处理的小鼠中，心脏中的甘油三酯显著富集。这些结果表明，PM10总和直接参与影响外周组织中的脂质代谢和氧化应激，这可能与空气污染对人类健康的严重全身影响有关。
