Periodontal Disease and Nuclear and Oxidative DNA Damage

Oral health is an important aspect of the overall health status of an individual. DNA damage has been associated with oral health and dental factors due to the increased of oxidative stress (OxS). DNA damage can produce a wide range of effects on human health. These effects could appear immediately, but others do not become evident much later. Chronic diseases have been study to understand their mechanisms, clinical implications, and the development of secondary disease such as cancer. Periodontitis is one of the most common oral diseases. It is an inflammatory chronic infectious disease, which is characterized by the loss of supporting tissues and tooth loss caused by periodontopathogens and long-term release of reactive oxygen species (ROS); thus, oxidative stress is increased during periodontitis. Oxidative stress can produce DNA damage, including the oxidation of nucleosides, which could cause DNA strand break. This oxidative damage leads the formation of micronuclei (MN) a marker of nuclear damage. Also, oxidative stress increased 8-hydroxy-2′-deoxyguanosine levels which are the most common stable product of oxidative DNA damage

Ultraviolet-A Light Induces Micronucleated Erythrocytes in Newborn Rats

Background: Ultraviolet-A (UV-A) light induce DNA damage by creating pyrimidine dimers, or indirectly affects DNA by the formation of reactive oxygen species. The objective was to determine DNA damage by micronucleus test in neonatal rats exposed to UV-A light. Methods: Rat neonates were exposed to light from a LED lamp (control group), to UV-C light 254 nm (control group to desquamation skin) or UV-A light 365 nm and in one group the dams were supplemented with folic acid (FA), to determine micro nucleated erythrocytes (MNE) and micro nucleated polychromatic erythrocytes (MNPCE) in peripheral blood of offspring. Results: All the rat neonates exposed to UV-C lamp showed desquamation skin, while for UV-A lamp no desquamation was observed, and there was MNE differences in all sampling times (P<0.02) and for MNPCE in 9 min group (P=0.001). No differences between the groups with and without FA were observed. Conclusion: Increased MNE frequencies without apparent damage to the skin could be induced with UV-A light exposure. Under these conditions, FA no protected against UV-A light exposure. This study shows a manner to quantify the genotoxic effects of UV-A light in peripheral blood erythrocytes of rat neonates