Shimin Zhanga,b, Xiang Lia, Fuwei Xiea, Kejian Liua, Huimin Liua, Jianping Xiea
a Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, Zhengzhou 450001, China
b Technique Center of Tobacco Production, PingDingshanTobacco Company of Henan Tobacco Monopoly Bureau, PingDingshan 467000, China
The purpose of this study is to evaluate oxidative stress induced by whole cigarette smoke based on the air-liquid interface exposure system. The cytotoxicity of whole smoke were measured by MTT and NRU assays, and several intracellular and extracellular oxidative stress biomarkers such as GSH and GSSG, MDA, HNE, EC-SOD and 8-OHdG were investigated in A549 and BEAS–2B cells.
A B S T R A C T
Cigarette smoke is a complex and oxidative aerosol. Previous researches on the hazards of cigarette smoke mainly focused on the adverse bioeffects induced by its condensates or gas vapor phase, which ignored the dynamic processes of smoking and the cigarette smoke aging. To overcome these disadvantages, we performed air-liquid interface exposure of whole smoke, which used native and unmodified smoke and ensured the exposure similar to physiological inhalation. Our results indicated that whole cigarette smoke induced lung epithelial cells (A549) and bronchial epithelial cells (BEAS-2B) damages in cytotoxicity assays (methyl thiazoly tetrazolium and neutral red uptake assays). In addition, A549 and BEAS–2B cells showed oxidative damages in whole smoke exposure, with concentration change of several biomarkers (reduced and oxidized glutathione, malondialdehyde, 4-hydroxyhydroxy-2-nonenal, extracellular superoxide dismutase, and 8-hydroxyl deoxyguanosine). These results indicate that whole smoke-induced oxidative stress occurs in two different kinds of cells at air-liquid interface.
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