Abstract
BACKGROUND: Cigarette smoke contains chemical components that cause excessive production of Reactive Oxygen Species (ROS), altering cell physiology and affecting key pathways. This leads to hyperinflammation, DNA damage, and cellular aging, which may cause oral and pulmonary pathologies. Our study aims to investigate the impact of smoking on ROS levels and cellular aging in oral mucosal cells. We compared Reactive oxygen Species and cellular aging between smokers and non-smokers. Secondarily, we also compared the results between young and old smokers. METHODS: Oral swabs were taken from 50 smokers and 50 nonsmokers using a cytology brush. We quantified the reactive oxygen species (ROS) by using oxidized 2'7' dichlorodihydrofluorescein-diacetate (DCFH-DA) dye. To assess cellular aging, mRNA levels of the CYR61 gene-a cellular aging marker, were compared through RT-PCR. RESULTS: It was found that smokers had a higher percentage of ROS in comparison to non-smokers (p value < 0.001). Additionally, there was an over-expression of the CYR61 gene in smokers as compared to non-smokers (p value = 0.001). Furthermore, when comparing ROS and cellular aging between young smokers and old smokers, it was noted that there was a significantly higher percentage of ROS and up-regulation of mRNA levels of CYR61 gene in young smokers in comparison to old smokers (p value 0.001 and <0.0001 respectively). CONCLUSION: It has been observed that smokers have a higher amount of ROS production and cellular aging in their oral mucosal cells. In young smokers, ROS and cellular aging were found to be higher compared to older smokers. This is quite concerning and could be a major factor leading to oral pathologies in smokers.