Abstract

The oral cancer is presumably caused by genetic factors and exposure to substances derived from cosmetics and disinfectants. Triclosan (TCS) is widely spread in many consumer products and oral care products. Since TCS can affect DNA methylation, which is one of the key mechanisms of gene expression that may lead to cancerogenesis, it is necessary to study this mechanism in oral cell carcinoma. The aim of the present study was to evaluate the impact of TCS on metabolic parameters, oxidative stress, gene expression, and DNA methylation and hydroxymethylation in the SCC-15 cell line. The experiments have shown TCS toxicity to SCC-15 cells only in the highest concentrations of 50 and 100 µM. TCS in a wide range of concentrations increases ROS production and caspase-3 activity. Our experiments have shown that TCS in the nontoxic concentrations of 10 µM exerts an impact on SOD2 mRNA expression and SOD activity in the SCC-15 cell line. Finally, our experiments have demonstrated that 6-h treatment with TCS decreases the mRNA expression of DNMT3A and DNMT3B. After 72-h exposure to TCS, an increased level of 5-methylcytosine and 5-hydroxymethylcytosine was observed in the SCC-15 cell line, but it was abolished by the NAC treatment. However, it is very likely that these results can be an effect of TET enzyme activity, especially in the case of the decrease in 5mC and the increase in 5hmC after the 48-h exposure to TCS, which was accompanied with a decrease in the mRNA expression of DNMT3A and DNMT3B.

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