The effects of Wakosil as a model of PM2.5 and/or Nicotine on Trace Elements Distribution in Lung Microvascular Endthelial Cells

[Speaker] Eiko Sakurai:1
[Co-author] Eiichi Sakurai:2, Shigeo Matsuyama:3, Keizo Ishii:3, Takahiro Satoh:4, Tomihiro Kamiya:5
1:Faculty of Pharmacy, Iwaki Meisei University, JPS, Japan, 2:Faculty of Pharmaceutical Sciences, Tokushima Bunnri University, Japan, 3:Department of Quantum Science and Energy Engineering, Tohoku University, Japan, 4:Department of Advanced Radiation Technology, TARRI, QST, Japan, 5:Department of Integrated Science and Technology, Gunma University, Japan

Background: It is well known that cigarette smoking is one of risk factors for lung. And air pollution is a serious problem all over the world. We think that combination of air pollutants and smoking are known serious risks to our health. Lung microvascular endothelial cells (LMECs) act as a barrier to protect from dangerous matters such as PM2.5 or cigarettes smoking. There are some reports that PM2.5 is an important etiologic factor for lung disease. However, there is no report on the cause of lung toxicity from PM2.5 and nicotine within the LMECs. Therefore, we investigated the effects of PM2.5 and/or cigarettes on LMECs by focusing on changes in intracellular trace elements levels.
Methods: We measured the changes of the LMEC demonstrated by the changes of its trace element levels, as a component captured by wakosil as a model. LMEC was treated by a time series of test components consisting of additing nicotine to Wacosil in 2, 5, 15 and 20 mins time interval. Changes to trace elements were detected by in-air micro-particle induced X-ray emission (micro-PIXE) method developed at TIARA. Micro-PIXE analyzed the spatial distribution of the elements quantitatively (pg-fg). Mice or rats LMECs were isolated using a modification of the technique described by Magee et al. LMEC was extracted from three-week old male C57BL/6J, ICR mice and SD rats purchased from Japan SLC.
Results: Trace elements in superoxide dismutase (SOD) such as copper, zinc nickel and chromium were detected in treated-nicotine LMECs. It was well known that SOD is an antioxidant-related enzyme. Thus nicotine in the cigarettes may promote reactive oxygen in the cells and induces LMECs apoptosis as demonstrated by the release of trace elements.
The effects of wakosil as a model of PM2.5 /nicotine on LMECs has produced less distribution change of trace elements, in comparison to nicotine-containing treatment. PM2.5 may not play a role in LMECs apoptosis on its own accord. Other air pollutants such as oxidative sulfa (SOx), oxidative nitrogen (NOx), bacteria and so on which stick on PM2.5 may play a major role in inducing LMECs apoptosis.

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