Effects of ambient PM2.5 on pathological injury, inflammation, oxidative stress, metabolic enzyme activity, and expression of c-fos and c-jun in lungs of rats

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• 作者：Ruijin Li ; Xiaojing Kou ; Lizhi Xie…
• 关键词：PM2.5 ; Rat lung injury ; Inflammation ; Proto ; oncogene ; Metabolic enzyme ; Oxidative stress
• 刊名：Environmental Science and Pollution Research
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：22
• 期：24
• 页码：20167-20176
• 全文大小：1,366 KB
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• 作者单位：Ruijin Li (1)
  Xiaojing Kou (1)
  Lizhi Xie (2)
  Fangqin Cheng (3)
  Hong Geng (1)
  
  1. Institute of Environmental Science, Shanxi University, 92 Wucheng Road, Taiyuan, 030006, Shanxi Province, People’s Republic of China
  2. Shanxi Qingyuan Environmental Consultation Co., Ltd, Taiyuan, People’s Republic of China
  3. State Environmental Protection Key Laboratory of Efficient Utilization of Coal Waste Resources, Shanxi University, 92 Wucheng Road, Taiyuan, 030006, Shanxi Province, People’s Republic of China
  
• 刊物类别：Earth and Environmental Science
• 刊物主题：Environment
  Environment
  Atmospheric Protection, Air Quality Control and Air Pollution
  Waste Water Technology, Water Pollution Control, Water Management and Aquatic Pollution
  Industrial Pollution Prevention
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1614-7499

文摘

Fine particulate matter (PM<sub>2.5sub>) exposure is associated with morbidity and mortality induced by respiratory diseases and increases the lung cancer risk. However, the mechanisms therein involved are not yet fully clarified. In this study, the PM<sub>2.5sub> suspensions at different dosages (0.375, 1.5, 6.0, and 24.0 mg/kg body weight) were respectively given to rats by the intratracheal instillation. The results showed that PM<sub>2.5sub> exposure induced inflammatory cell infiltration and hyperemia in the lung tissues and increased the inflammatory cell numbers in bronchoalveolar lavage fluid. Furthermore, PM<sub>2.5sub> significantly elevated the levels of pro-inflammatory mediators including tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β, and intercellular adhesion molecule 1 (ICAM-1) and the expression of c-fos and c-jun in rat lungs exposed to higher dose of PM<sub>2.5sub>. These changes were accompanied by decreases of activities of superoxide dismutase and increases of levels of malondialdehyde, inducible nitric oxide synthase, nitric oxide, cytochrome P450s, and glutathione S-transferase. The results implicated that acute exposure to PM<sub>2.5sub> induced pathologically pulmonary changes, unchained inflammatory and oxidative stress processes, activated metabolic enzyme activity, and enhanced proto-oncogene expression, which might be one of the possible mechanisms by which PM<sub>2.5sub> pollution induces lung injury and may be the important determinants for the susceptibility to respiratory diseases. Keywords PM<sub>2.5sub> Rat lung injury Inflammation Proto-oncogene Metabolic enzyme Oxidative stress