Repeated Intratracheal Instillation of PM10 Induces Lipid Reshaping in Lung Parenchyma and in Extra-Pulmonary Tissues

Abstract

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.

In Vivo Comparative Study on Acute and Sub-acute Biological Effects Induced by Ultrafine Particles of Different Anthropogenic Sources in BALB/c Mice

“…Instead, mice subjected to three repeated instillations of 50 μg UFPs/instillation every three days are consider representative of a sub-acute exposure (Figure 9B) [30,31,32,78]. Three h after a single instillation or 24 h after the last instillation of the repeated exposure protocol, mice of each experimental group (sham, BB and DEP-treated) were anesthetised by gas to minimize suffering and euthanized with cervical dislocation.…”

“…Here we present a comparative in-vivo study aimed to elucidate the putative differences between the responses elicited by UFPs derived from diverse anthropogenic sources (DEP and BB). Intratracheal instillation of particulate matter in BALB/c mice is a useful and validated in-vivo model to study pollutants induced toxicity [30,31,32]. Therefore, we analyzed in this model how a short-term exposure or repeated exposures to DEP or BB could differently affect a panel of pro-inflammatory, cytotoxic, and oxidative stress markers in bronchoalveolar lavage fluid (BALf), lung and heart parenchyma, since they may not share the same biological mechanisms [33].…”

Exposure to Airborne Particulate Matter: An Additional Risk Factor for Metabolic Syndrome in Saudi Arabia

“…The association between exposure to PM exposure and the individual components of MetS such as: Hyperglycemia, hypertension, high triglycerides, obesity and low HDL has been well documented in literature (Li, et al, 2013;Roberts, et al, 2014;Rizzo, et al, 2014;Wang, et al, 2014;Fleisch, et al, 2014 andPope, et al, 2015) . However, studies relating MetS per se with PM exposure are scarce.…”

PM2.5induces embryonic growth retardation: Potential involvement of ROS-MAPKs-apoptosis and G0/G1 arrest pathways

“…Various mechanisms have been proposed for the adverse health effects of PM, including inflammatory responses, endotoxin effects, pro‐coagulant effects and ROS production (Li et al, ; Rizzo et al, ). Among these, the intracellular generation of ROS has been considered to be the common mechanism by which PM may trigger various signaling pathways and lead to different adverse effects (Soberanes et al, ).…”