The study published in the journal BMC Cell Biology this week may begin to explain why. According to the findings, when cells are exposed to smoke, their ability to move toward the site of damage is compromised.
The study, led by Professor Manuela Martins-Green, of the Department of Cell Biology and Neuroscience and her student Lina Wong, examined the effects of second-hand smoke on fibroblasts, cells that play a major role in wound healing. The UC Riverside research team also included graduate student Jo Ellen Feugate, undergraduate researcher Harry Miguel Green of Dr. Martins-Green's group, Professor Eugene A Nothnagel and Staff Research Associate Madhav Yadav of the Department of Botany and Plant Sciences.
In second-hand smoke, many components are more concentrated than in first-hand smoke. For example, the concentrations of nicotine, tar, nitric oxide and carbon monoxide levels are at least twice as high as those the smoker inhales.
Among the findings, they discovered that exposure to smoke altered the arrangement of the cells' cytoskeleton - increasing the cells' adhesive properties and thus reducing their mobility.
The research team bubbled smoke from the lit end of cigarettes through cell culture media to form a solution containing the major components of second-hand smoke. They then diluted the 'smoky media' until the smoke components reached the levels found in the tissues of passive smokers.
When they added this media to fibroblast cells cultured in vitro, the researchers saw that the cells became more elongated and that they separated from one another. By studying components of the cytoskeleton in more detail, the researchers saw that exposure to smoke increased the level of one particular cytoskeletal component, actin, inside t
Contact: Ricardo Duran
University of California - Riverside