The mechanisms underlining the cell adaptive and/or activating oxidative stress, called low level light or photobiomodulation therapies (PBMT), still remain unclear for the near-infrared spectrum range (750-3000 nm), especially for the 1265-1270 nm range (highest absorption by molecular oxygen). It is most probable that the mitochondria may also appear to be the main target for these wavelengths. It is known that mitochondria can generate ROS under visible and 800-1060 nm spectrum range irradiation, which in turn control voltage-dependent anion channels (VDAC). Here we investigated cellular damage regarding VDAC activity, level of oxidative stress, malondialdehyde content, cell viability, mitochondrial potential and mass, GSH level, mitochondrial and nuclear DNA damage in the cancer cell culture exposed to low-level laser irradiation at 1265 nm. We used a continuous wave laser with output power 4 mW; the energy densities employed were 0.3-9.45 J/cm 2. We observed that the laser radiation at 1265 nm can induce the oxidative stress, enhance apoptosis, and disturb mitochondrial functioning at the energy density of 9.54 J/cm 2. In addition, inhibition of VDAC enhances the observed effects. It has been shown that the laser irradiation at 1265 nm damages mitochondrial DNA but does not affect the nuclear DNA. The performed experiments bring us to the conclusion that the laser irradiation at 1265 nm can affect cells through mitochondrial damage and the inhibition of VDAC enhances effects of PBMT.
|Journal||IEEE Journal of Selected Topics in Quantum Electronics|
|Early online date||12 Jul 2018|
|Publication status||Published - 1 Jan 2019|
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- cancer cell
- near-infrared lasers
- photobiomodulation therapy