Role of tobacco smoke on lung response to crystalline silica exposure in rats

Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of lung toxicity in response to crystalline silica exposure. Nevertheless, the precise role of tobacco smoke exposure on the lung response to tobacco smoke exposure and the underlying mechanisms remain largely elusive. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary toxicity and the underlying molecular mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in rats exposed to air, crystalline silica, tobacco smoke, or crystalline silica plus tobacco smoke. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by tobacco smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to tobacco smoke, silica or a combination of both compared with the air exposed control rats.既往研究表明，吸烟可诱发氧化应激与炎症反应——二者均为结晶二氧化硅（crystalline silica）暴露所致肺毒性发生与进展的相关已知因素。然而，烟草烟雾暴露对肺部针对结晶二氧化硅暴露的应答的具体作用及其潜在机制，目前仍不甚明确。因此，本研究旨在探讨吸烟（若存在影响）对二氧化硅诱导的肺毒性的作用及其潜在分子机制。本研究对暴露于空气、结晶二氧化硅、烟草烟雾或二者联合暴露的大鼠的肺毒性及肺部基因表达谱进行了检测。结果显示，二氧化硅暴露可引发显著的肺毒性，而烟草烟雾暴露会进一步加重大鼠的该肺损伤。与空气暴露的对照组大鼠相比，烟草烟雾暴露组、二氧化硅暴露组及二者联合暴露组大鼠的肺部基因表达谱均存在显著差异。