Low level laser radiation at 1265 nm triggers cellular effects through mitochondrial damage

Abstract

The mechanism responsible for the oxidative stress induction due to laser irradiation at 1265-1270 nm is still unclear. Thermal effects caused by irradiation are the main factors to be eliminated. In this study, low-level laser radiation (LLLI) has been used at 1265 nm to avoid side effects associated with the thermal denaturation of biomolecules and provide conditions that at least theoretically exclude singlet oxygen generation by direct 3O2 → 1O2 transition. Here, we report on the experimental results highlighting mitochondrial role in the oxidative stress provoked by LLLI within the wavelength range 1260-1275 nm. We study the dynamics of oxidative stress, mitochondrial potential, cardiolipin oxidation, cell death, mitochondrial and nuclear DNA damage in the HCT-116 cell line exposed to low-level laser irradiation at 1265 nm. We demonstrate that the laser radiation at 1265 nm can induce the oxidative stress and disturb mitochondrial functioning at the energy density as low as 3.15 J/ cm2 and 9.45 J/cm2, respectively. Noteworthy, LLLI at 1265 nm damages mitochondrial DNA but does not affect the nuclear DNA. The performed experiments brought us to the conclusion that the laser irradiation at 1265 nm can affect intracellular processes through mitochondrial damage.