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The damage of NO2 inhalation exposure to myocardial cell mitochondria in rats(PDF)

Chinese Journal of Applied & Environmental Biology[ISSN:1006-687X/CN:51-1482/Q]

2014 06
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The damage of NO2 inhalation exposure to myocardial cell mitochondria in rats
HOU Meiyi SANG Nan
College of Environmental and Resource Sciences, Shanxi University, Taiyuan 030006, China
NO2 myocardial mitochondria PGC-1α NRF1 TFAM CVD

The heart is suggested to be one of the important target organs of nitrogen dioxide (NO2) besides the respiratory system. Since effective operation of the heart is based on mitochondria, it is of great significance to study the correlation between NO2 pollution and mitochondrial structure and function for prevention and intervention of cardiovascular diseases (CVD) after NO2 exposure. In the present study, we established NO2 inhalation exposure model using Wistar rats with chronic (control, 1 × 10-6, 2.5 × 10-6) and acute (control, 2.5 × 10-6, 5 × 10-6, 10 × 10-6) exposure, to investigate the mitochondrial ultrastructure of myocardial cell. The mitochondrial function was detected by membrane potential and activity. The protein levels of mitochondrial respiratory chain transcription factors PGC-1α, NRF1, and TFAM were assayed by Western blot. The results showed a decrease of the number of mitochondria and swelling of myocardial cells after chronic and low concentration NO2 exposure. The mitochondria activity declined significantly, being 0.79 times (P < 0.05) and 0.56 times (P < 0.05) respectively of the control. The membrane potential was significantly lower, being 0.89 times (P < 0.05) and 0.79 times (P < 0.05) respectively of the control. Expressions of PGC-1α, NRF1 and TFAM declined significantly to 76% (P < 0.05), 85% (P < 0.001) and 52% (P < 0.05) respectively in myocardial cell after 2.5 × 10-6 chronic and low concentration NO2 exposure. However, after acute and high concentration NO2 stimulation the number of myocardial cell mitochondria increased. The mitochondria activity increased to 1.52 (P < 0.001) and 2.12 (P < 0.001) times respectively with 5 × 10-6 and 10 × 10-6 NO2. The membrane potential increased significantly to 1.50 (P < 0.05), 1.62 (P < 0.05) and 2.25 (P < 0.001) times respectively with 2.5 × 10-6, 5 × 10-6 and 10 × 10-6 NO2. The expression levels of PGC-1α, NRF1 and TFAM all increased significantly in myocardial cell of rats, to 1.51 (P < 0.001), 1.47 (P < 0.05) and 1.60 (P < 0.001) times respectively under 10×10-6 exposure. The results indicated that chronic and low concentration NO2 exposure causes mitochondrial dysfunction by myocardial mitochondria oxidative phosphorylation weakening. Meanwhile, the opposite biological effect after acute and high concentration NO2 stimulation could be due to the compensative effect. The mitochondrial structure and function damage might be one of the molecular mechanisms of CVD induced by NO2 pollution.


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