Oxidative damage to lung tissue and peripheral blood in endotracheal PM2.5-treated rats.

نویسندگان

  • Zhi-Qing Lin
  • Zhu-Ge Xi
  • Dan-Feng Yang
  • Fu-Huan Chao
  • Hua-Shan Zhang
  • Wei Zhang
  • Huang-Liang Liu
  • Zai-Ming Yang
  • Ru-Bao Sun
چکیده

OBJECTIVE To investigate the oxidative damage to lung tissue and peripherial blood in PM2.5-treated rats. METHODS PM2.5 samples were collected using an auto-sampling instrument in summer and winter. Treated samples were endotracheally instilled into rats. Activity of reduced glutathione peroxidase (GSH-Px) and concentration of malondialdehyde (MDA) were used as oxidative damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. DNA migration length (microm) and rate of tail were used as DNA damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. RESULTS The activity of GSH-Px and the concentration of MDA in lung tissue significantly decreased after exposure to PM2.5 for 7-14 days. In peripheral blood, the concentration of MDA decreased, but the activity of GSH-Px increased 7 and 14 days after experiments. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. The DNA migration length (microm) and rate of tail in lung tissue and peripheral blood significantly increased 7 and 14 days after exposure to PM2.5. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. CONCLUSION PM2.5 has a definite oxidative effect on lung tissue and peripheral blood. The activity of GSH-Px and the concentration of MDA are valuable biomarkers of oxidative lung tissue damage induced by PM2.5. The DNA migration length (microm) and rate of tail are simple and valuable biomarkers of PM2.5-induced DNA damage in lung tissues and peripheral blood. The degree of DNA damage in peripheral blood can predict the degree of DNA damage in lung tissue.

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عنوان ژورنال:
  • Biomedical and environmental sciences : BES

دوره 22 3  شماره 

صفحات  -

تاریخ انتشار 2009