BACKGROUND: Cigarette smoke extract (CSE), a model for studying the effects of tobacco smoke in vivo and in vitro, induces cell oxidative stress and affects the antioxidative glutathione system. We evaluated the impact of CSE on airway epithelial cells and the possible cytoprotective effect of the mucolitic drug S-carboximethilcysteine lysine salt (S-CMC-Lys). METHODS: Reduced glutathione (GSH) and reactive oxygen species (ROS) intracellular levels were evaluated by fluorimetry in human bronchial epithelial cells (16-HBE) and the expression and activity of enzymes of the GSH metabolic pathway were investigated by RT-PCR, Western blot and colorimetric assays. RESULTS: CSE significantly increased cell mortality in a time and dose dependent manner, via an apoptosis-independent pathway. Short-term (3 hours) CSE exposure induced an increase in ROS levels and a GSH intracellular concentration drop. In parallel, the expression of glutathione peroxidases 2 and 3, glutathione reductase and glutamate-cysteine-ligase was increased. S-CMC-Lys was effective in counteracting these effects. CONCLUSION: CSE affects ROS levels, GSH concentration and GSH enzymes pathway. These effects can be to some extent reversed by S-CMC-Lys, that could represent a therapeutic tool to counteract CSE induced oxidative cellular injuries.
BACKGROUND: Cigarette smoke extract (CSE), a model for studying the effects of tobacco smoke in vivo and in vitro, induces cell oxidative stress and affects the antioxidative glutathione system. We evaluated the impact of CSE on airway epithelial cells and the possible cytoprotective effect of the mucolitic drug S-carboximethilcysteine lysine salt (S-CMC-Lys). METHODS: Reduced glutathione (GSH) and reactive oxygen species (ROS) intracellular levels were evaluated by fluorimetry in human bronchial epithelial cells (16-HBE) and the expression and activity of enzymes of the GSH metabolic pathway were investigated by RT-PCR, Western blot and colorimetric assays. RESULTS: CSE significantly increased cell mortality in a time and dose dependent manner, via an apoptosis-independent pathway. Short-term (3 hours) CSE exposure induced an increase in ROS levels and a GSH intracellular concentration drop. In parallel, the expression of glutathione peroxidases 2 and 3, glutathione reductase and glutamate-cysteine-ligase was increased. S-CMC-Lys was effective in counteracting these effects. CONCLUSION: CSE affects ROS levels, GSH concentration and GSH enzymes pathway. These effects can be to some extent reversed by S-CMC-Lys, that could represent a therapeutic tool to counteract CSE induced oxidative cellular injuries.
Authors: Fabio Bucchieri; Antonella Marino Gammazza; Alessandro Pitruzzella; Alberto Fucarino; Felicia Farina; Peter Howarth; Stephen T Holgate; Giovanni Zummo; Donna E Davies Journal: PLoS One Date: 2015-03-20 Impact factor: 3.240
Authors: Arunava Ghosh; Sabri H Abdelwahab; Steven L Reeber; Boris Reidel; Abigail J Marklew; Andrew J Garrison; Shernita Lee; Hong Dang; Amy H Herring; Gary L Glish; Mehmet Kesimer; Robert Tarran Journal: Sci Rep Date: 2017-04-27 Impact factor: 4.379
Authors: Longjie Zhang; Min Ning; Yingbo Xu; Chenghui Wang; Guangshan Zhao; Qingqing Cao; Jinsong Zhang Journal: Int J Environ Res Public Health Date: 2016-03-21 Impact factor: 3.390
Authors: Sneh Koul; Victoria L Schaal; Subhash Chand; Steven T Pittenger; Neetha Nanoth Vellichirammal; Vikas Kumar; Chittibabu Guda; Rick A Bevins; Sowmya V Yelamanchili; Gurudutt Pendyala Journal: Cells Date: 2020-08-11 Impact factor: 6.600