Cell survival, DNA, and protein damage in B14 cells under low-intensity near-infrared (810 nm) laser irradiation.

ABSTRACT

OBJECTIVE: The aim of this study was to reveal the possible cytotoxic and genotoxic effects of low-intensity (200 mW) near-infrared (810 nm) laser irradiation, using B14 cell line. BACKGROUND DATA Laser therapy is widely used in biomedical treatment of many diseases, but the possible molecular mechanisms of laser actions remain unclear and the damaging effects of laser irradiation are still controversial. The side effects of laser therapy involve the generation of reactive oxygen and nitrogen species which in turn initiate lipid peroxidation, protein damage or DNA modification. METHODS: B14 cells and suspension of human erythrocyte membranes were irradiated with near-infrared (810 nm) therapy laser at different radiant exposures (3.75-15.0 J/cm(2)) and light power (fluency rate) 200 mW at 22 degrees C. Laser induced cellular oxidative damage was measured in terms of cell survival, DNA damage, measured using the method of single cell gel electrophoresis (Comet assay), protein damage measured as protein carbonyls formation. RESULTS: No substantial changes of cell survival under B14 cells irradiation at radiant exposures 3.75-11.25 J/cm(2) were observed. Similarly, neither considerable light-induced DNA damage or protein carbonyls accumulation was revealed. On the contrary, laser irradiation has led to decrease of cell protein carbonyl groups level in a dose-dependent manner. Additionally, using human red blood cell membranes as model membranes and biological oxidant HOCl we observed that laser irradiation resulted in a decrease of the level of membrane protein carbonyl groups accumulated under oxidative HOCl treatment. CONCLUSIONS: We can conclude that laser irradiation used (810 nm, 200 mW, 3.75-11.25 J/cm(2)) did not produce any considerable cytotoxic or genotoxic effects in B14 cells. Moreover, laser irradiation reduced cellular protein damage (protein carbonyl groups) produced by biological oxidant HOCl.