Response of human oral epithelial cells to oxidative damage and the effect of vitamin E.
Smoking and periodontal inflammation are various conditions with the potential to induce oxidative stress and thus DNA damage in the oral cavity. In cellular defense systems, vitamin E is considered the most powerful lipid-soluble antioxidant. To investigate whether oxygen-free radicals alter normal progression of the cell cycle and whether vitamin E prevents this damage, we exposed cultured normal human oral epithelial cells to hydrogen peroxide (H2O2) in the presence or absence of vitamin E. Two primary cell lines were analyzed for the presence of hydroxyl radical, cell cycle distribution and morphology. Each cell line received five treatments: control, ethanol only, vitamin E only, H2O2 only or vitamin E followed by H2O2. Degradation of hydroxyl radicals was detected by electron paramagnetic resonance analysis, cell cycle by flow cytometry and morphology by organotypic technique. Hydroxyl radicals were generated in H2O2-treated cells at an initial concentration, which decreased over a period of time. Cell cycle analysis showed that H2O2-treated cells differed from normal cells in that the percentage of cells in the G1 phase decreased markedly (34.3 vs. 61.2% in control) and the S phase increased (35.5 vs. 15.6% in control). Organotypic cultures treated with H2O2 demonstrated nuclear hyperchromatism, loss of maturation and prominent nucleoli, features consistent with premalignant epithelial transformation. In conclusion, our data suggest that H2O2 produced hydroxyl radicals and altered the cell cycle. Also, vitamin E may have the potential to reduce oxidative damage caused by hydroxyl radicals.
Royack
G A
GA
Department of Oral and Maxillofacial Surgery, School of Dentistry, University of Washington, Seattle, USA.
Nguyen
M P
MP
Tong
D C
DC
Poot
M
M
Oda
D
D
D004847:Epithelial Cells / Q000187:drug effects; D006801:Humans; D006861:Hydrogen Peroxide / Q000009:adverse effects*; D009059:Mouth Diseases / Q000139:chemically induced* / Q000473:pathology; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D014810:Vitamin E / Q000627:therapeutic use*
D014810:Vitamin E; D006861:Hydrogen Peroxide