Higher Reactive Oxygen Species and cellular aging in oral mucosal cells of young smokers: a comparative analytical study.

IF 3.1 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Frontiers in oral health Pub Date : 2025-02-14 eCollection Date: 2025-01-01 DOI:10.3389/froh.2025.1372494
Bushra Imdad, Uzair Abbas, Pershad Kumar, Durre Sameen Kamran, Mahtab Khan, Niaz Hussain, Muhib Ullah Khalid
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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.

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较高的活性氧和细胞老化的口腔粘膜细胞的年轻吸烟者:比较分析研究。
背景:香烟烟雾中含有的化学成分会导致活性氧(ROS)的过量产生,改变细胞生理并影响关键途径。这会导致过度炎症、DNA损伤和细胞老化,从而导致口腔和肺部病变。本研究旨在探讨吸烟对口腔黏膜细胞ROS水平和细胞衰老的影响。我们比较了吸烟者和非吸烟者的活性氧和细胞老化。其次,我们还比较了年轻吸烟者和老年吸烟者之间的结果。方法:用细胞学刷取50例吸烟者和50例非吸烟者的口腔拭子。我们用氧化的2‘7’二氯双氢荧光素-二乙酸(DCFH-DA)染料定量测定活性氧(ROS)。为了评估细胞衰老,通过RT-PCR比较CYR61基因(细胞衰老标志物)的mRNA水平。结果:吸烟者的ROS百分比高于非吸烟者(p值p值= 0.001)。此外,当比较年轻吸烟者和老年吸烟者之间的ROS和细胞衰老时,我们注意到,与老年吸烟者相比,年轻吸烟者的ROS百分比和CYR61基因mRNA水平的上调明显更高(p值0.001)。结论:我们观察到吸烟者口腔粘膜细胞中ROS的产生量和细胞衰老量更高。在年轻吸烟者中,活性氧和细胞老化被发现比老年吸烟者更高。这是非常令人担忧的,可能是导致吸烟者口腔病变的主要因素。
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CiteScore
3.30
自引率
0.00%
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0
审稿时长
13 weeks
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