E-cigarettes and Oral Cell Damage

Objectives: The purpose of this study is to provide scientific evidence of the effect ecigarette smoke has on oral cells by measuring mitochondrial function, as it is highly sensitive to enviromental toxins, and mitochondrial dysfunction may promote the onset of cancer .
Methods: Human gingival fibroblast (HGF-1) cells were exposed to e-cigarette smoke extract media at different concentrations and time points. We measured the NAD+/NADH ratio using a colometric assay to show any changes associated with cell toxicity and mitochondrial function at each time and concentration. We also measured MT-COX1 ((Mitochondrially Encoded Cytochrome C Oxidase I) and SHA (encoded in the nucleus) using western blot to measure regulation of mitochondrial biogenesis and cellular stress response to the vape extraction.
Results: Our preliminary data suggests that the higher the concentration and the longer the time the cells are exposed to e-cigarette, the higher is the damage effect of the mitochondrial function. It coud be seen as the NAD+/NADH ratio changed through time, as well as the expresion of the succinate dehydrogenase subunit A (SDHA) and cytochrome c oxidase subunit I.
Conclusions: E-cigarette exposure to oral cells induces changes in mitochondrial respiration and metabolism, oxidant generation, mitochondrial DNA (mtDNA) damage and dysfunctioanl reduction-oxidation (redox) signaling. These changes may lead to a long to midterm cell transformation that could potentially lead towards cancer.