| Effects of Nicotine, Cotinine and Benzopyrene as Smoke Components on the Expression of Antioxidants in Human Bronchial Epithelial Cells. |
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Yong Seok Kim, Jae Hyung Lee, Sang Heon Kim, Tae Hyung Kim, Jang Won Sohn, Ho Joo Yoon, Sung Soo Park, Dong Ho Shin |
1Department of Internal Medicine, College of Medicine, Hanyang University, Seoul, Korea. shindh@hanyang.ac.kr
2Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea. |
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| Abstract |
BACKGROUND
Cigarette smoking is an important risk factor for chronic bronchitis and COPD. Airway epithelial cells exposed to cigarette smoke components such as nicotine, cotinine and benzopyrene can generate reactive oxygen species (ROS) and be subject to oxidative stress. This oxidative stress can induce the inflammatory response in the lung by the oxidant itself or by the release of proinflammatory cytokines. It has been reported that nicotine stimulates ROS, which are associated with NF-kappaB. METHODS: Beas2B cells were treated with nicotine, cotinine and benzopyrene. RT PCR was used to measure the expression of several antioxidant factors using the total RNA from the Beas2B cells. The level of superoxide dismutase(CuZnSOD), thioredoxin, glutathione reductase expression was examined. RESULTS: 0.5 to 4 hours after the benzopyrene, nicotine and cotinine theatments, the level of thioredoxin and glutathione reductase expression decreased. Longer exposure to these compounds for 24 to 72 hours inhibited the expression of most of these antioxidant factors. CONCLUSION: During exposure to smoke compounds, thioredoxin and glutathione reductase are the key antioxidant factors induced sensitively between 0.5 and 4 hours but the levels these antioxidants decrease between 24 hour and 72hours. |
| Key Words:
Beas2B cell, Benzopyrene, Nicotine, Cotinine, Antioxidants |
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