Imdad Bushra, Abbas Uzair, Kumar Pershad, Kamran Durre Sameen, Khan Mahtab, Hussain Niaz, Khalid Muhib Ullah
Department of Physiology, Dow University of Health Sciences, Karachi, Pakistan.
Department of Pulmonology, Jinnah Postgraduate Medical Center, Karachi, Pakistan.
Front Oral Health. 2025 Feb 14;6:1372494. doi: 10.3389/froh.2025.1372494. eCollection 2025.
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.
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.
It was found that smokers had a higher percentage of ROS in comparison to non-smokers ( value < 0.001). Additionally, there was an over-expression of the CYR61 gene in smokers as compared to non-smokers ( 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 ( value 0.001 and <0.0001 respectively).
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.
香烟烟雾中含有能导致活性氧（ROS）过度产生的化学成分，从而改变细胞生理并影响关键途径。这会导致炎症反应过度、DNA损伤和细胞衰老，进而可能引发口腔和肺部疾病。我们的研究旨在调查吸烟对口腔黏膜细胞中ROS水平和细胞衰老的影响。我们比较了吸烟者和非吸烟者之间的活性氧和细胞衰老情况。其次，我们还比较了年轻吸烟者和老年吸烟者的结果。
使用细胞学刷从50名吸烟者和50名非吸烟者中采集口腔拭子。我们使用氧化型2'7'二氯二氢荧光素二乙酸酯（DCFH-DA）染料对活性氧（ROS）进行定量。为了评估细胞衰老，通过逆转录聚合酶链反应（RT-PCR）比较了细胞衰老标志物CYR61基因的mRNA水平。
发现吸烟者的ROS百分比高于非吸烟者（ 值<0.001）。此外，与非吸烟者相比，吸烟者中CYR61基因存在过表达（ 值=0.001）。此外，在比较年轻吸烟者和老年吸烟者之间的ROS和细胞衰老时，发现与老年吸烟者相比，年轻吸烟者的ROS百分比显著更高，且CYR61基因的mRNA水平上调（ 值分别为0.001和<0.0001）。
据观察，吸烟者口腔黏膜细胞中的ROS产生量和细胞衰老程度更高。在年轻吸烟者中，发现ROS和细胞衰老比老年吸烟者更高。这相当令人担忧，可能是导致吸烟者口腔疾病的一个主要因素。
