Photodynamic therapy is the main technique applied for surface carcinoma treatment. This technique employs singlet oxygen generated via a laser excited photosensitizer as a main damaging agent. However, prolonged sensitivity to intensive light, relatively low tissue penetration by activating light the cost of photosensitizer (PS) administration can limit photodynamic therapy applications. Early was reported singlet oxygen generation without photosensitizer induced by a laser irradiation at the wavelength of 1250-1270 nm. Here, we study the dynamics of oxidative stress, DNA damage, changes of mitochondrial potential, and mitochondrial mass induced by a laser at 1265 nm have been studied in HCT-116 and CHO-K cells. Laser irradiation of HCT-116 and CHO-K cells has induced a dose-dependent cell death via increasing intracellular reactive oxygen species (ROS) concentration, increase of DNA damage, decrease of mitochondrial potential, and reduced glutathione. It has been shown that, along with singlet oxygen generation, the increase of the intracellular ROS concentration induced by mitochondrial damage contributes to the damaging effect of the laser irradiation at 1265 nm.

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The mechanisms underlining the cell adaptive and/or activating oxidative stress called low level light (LLLT) or photobiomodulation therapies (PBMT) still remain unclear for near-infrared (NIR) spectrum range (750-3000 nm) especially for 1265-1270 nm range (highest absorption by molecular oxygen). It is most probably 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 caused by low doses of 1265-70 nm laser radiation regarding to VDAC activity, the level of oxidative stress, malondialdehyde (MDA) 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 continuous wave laser with output power 4 mW, the energy 

Here at the first time we suggested that the surface plasmon-polariton phenomenon which it is well described in metallic nanostructures could also be used for explanation of the unexpectedly strong oxidative effects of the low-intensity laser irradiation in living matters (cells, tissues, organism). We demonstrated that the narrow-band laser emitting at 1265 nm could generate significant amount of the reactive oxygen species (ROS) in both HCT116 and CHO-K1 cell cultures. Such cellular ROS effects could be explained through the generation of highly localized plasmon-polaritons on the surface of mitochondrial crista. Our experimental conditions, the low-intensity irradiation, the narrow spectrum band (<4 nm) of the laser and comparably small size bio-structures (~10 μm) were shown to be sufficient for the plasmon-polariton generation and strong laser field confinement enabling the oxidative stress observed.

The interaction of a surface plasmon polariton wave of the far-infrared regime propagating in a single-walled carbon nanotube with a drift current is theoretically investigated. It is shown that under the synchronism condition a surface plasmon polariton amplification mechanism is implemented due to the transfer of electromagnetic energy from a drift current wave into a terahertz surface wave propagating along the surface of a single-walled carbon nanotube. Numerical calculations show that for a typical carbon nanotube surface plasmon polariton amplification coefficient reaches huge values of the order of 10 сm, which makes it possible to create a carbon-nanotube-based spaser.