DNA Damage Caused by Oral Malodorous Compounds in Periodontal Cells In Vitro: Novel Carcinogenic Pathway
As a result of mitochondrial or active-oxygen scavenger insults, intracellular levels of reactive oxygen species (ROS) increase. These changes can induce DNA alterations in double- or single-strand DNA. DNA damage can be found in a wide variety of systemic or local diseases such as cardiovascular and neurodegenerative conditions, as well as in inflammation or infection. High levels of ROS together with DNA damage are also encountered in many human cancer types. Cellular response to DNA damage involves complex molecular pathways that represent the cell’s defensive system against DNA mutations. Depending on the amount of DNA damage accumulated, the cell will trigger DNA repair, cell-cycle arrest, or apoptosis.
Hydrogen sulfide (H2S) is a volatile organic compound responsible for physiological halitosis. Several studies have focused on the pathogenic role of H2S in the initiation and development of periodontitis. H2S has been shown to increase the ROS levels and to cause DNA damage in a number of cell types derived from oral tissues, such as oral fibroblasts, normal oral keratinocytes, oral keratinocyte stem cells, and osteoblasts. H2S may have an important role in the aging or carcinogenesis in oral tissues caused by DNA damage. The present chapter reviews the available scientific evidence related to the genotoxic effects of H2S in the oral environment.
KeywordsPeroxide Sulfide Superoxide Electrophoresis Cytosol
- 5.Yaegaki K (1995) Oral malodor and periodontal disease. In: Rosenberg M (ed) Bad breath: research perspectives. Ramot Publishing-Tel Aviv University, Tel Aviv, pp 87–108Google Scholar
- 16.Meek DW (2009) Tumor suppression by p53: a role for the DNA damage response? Nat Rev Cancer 10:714–723Google Scholar
- 20.Calenic B, Yaegaki K, Ishkitiev N, Kumazawa Y, Imai T, Tanaka T (2013) p53-Pathway activity and apoptosis in hydrogen sulfide-exposed stem cells separated from human gingival epithelium. J Periodontal Res 48:322–330Google Scholar