Oxidative Damage to Lung Tissue and Peripheral Blood

Oxidative Damage to Lung Tissue and Peripheral Blood in Endotracheal PM2.5-treated Rats

INTRDUCTION Attention has been paid to the relation betweenenvironmental pollution by atmospheric article matters and human health in recent years. Fine particle matters (PM2.5) are thought to be the most hazardous air pollutants not only because of their high concentration in atmosphere but also because of them carrying many kinds of metal and organic elements.

They can penetrate bronchiole,pulmonary alveoli, and blood circulation due their small size and produce serious biological toxicity. Some serious diseases such as irritable asthma, leukemia, lung cancer, and cardiovascular diseases, are related with the pollution of PM2.5. So far, the multipathogenic mechanisms of PM2.5 are not well understood.

In an attempt to study the oxidative damage induced by PM2.5 in animals, we used the activity of GSH-Px and the concentration of MDA as biomarkers and the levels of these biomarkers in lung tissue and peripheral blood of rats exposed to PM2.5 by endotracheal instillation were determined.

The resulting oxidative DNA damage may be implicated in cancer risk and serve as a marker of oxidative stress relevant to other ailments caused by particulate air pollution. There are various preparations of ambient air PM2.5 inducing oxidative DNA damage in vitro systems, whereas in vivo studies are scarce.

Oxidative stress-induced DNA damage appears to an important mechanism of action of urban particulate air pollution. In an attempt to study the DNA damage induced by PM2.5 in animals, we used the DNA migration length and the rate of tail as biomarkers, and measured their levels in lung tissue and peripheral blood of rats exposed to PM2.5 by endotracheal instillation. In addition, the molecular mechanism of PM2.5 on health effects was explored.

MATERIALS AND METHODS Male rats Endotracheal instillation Detection of oxidative damage in lung tissueand peripheral blood (GSH-Px and MDA detecting kit) Detection of DNA damage in lung tissue and peripheral blood (Comet assay)

RESULTS The GSH-PX and MDA activities werelower than control group. The DNA migration and rate of tail were higher than control group.

DISCUSSION PM2.5 increases ROS production in lung cells andchronic PM2.5 exposure might create an oxidative stress within cells, particularly in mitochondria. Furthermore, chronic exposure to PM2.5 decreases the production of mitochondrial antioxidants, which may also lead to increased susceptibility to oxidative mitochondrial injury. Proteins are readily oxidized by ROS and may represent a critical target of oxidative damage within lung cells because oxidative inactivation of proteins could have very rapid and detrimental effects on cell viability due to their catalytic function.

In addition, PAH and phenol absorbed on PM2.5 can produce FOR during their metabolism to cause cell oxidative damage. At the same time, some physical

action of itself can concentrate neutrophilic granulocytes to lung and trachea to produce mass FOR which can cause physiological and pathological changes, even nucleic acid damage.

conclusion Our study provides data needed to guide additionaltoxicity studies and to support the design of environmental hygiene procedures. PM2.5 causes serious health hazard in animals and exposures to PM2.5 should be avoided. Although it is generally believed that particulate matters, especially PM2.5, threaten health, their toxic components and biological mechanisms involved remain unclear.

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