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.

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 mechanism responsible for the oxidative stress due to photobiomodulation induced by 1265 nm laser is still unclear. Mitochondria are assumed to be the most probable acceptors of the 1265 nm laser irradiation. We study oxidative stress, mitochondrial potential, GSH, cell viability, DNA damage. We demonstrated that narrowband (highcoherent) and wideband lasers employed at the doses of 9.45 and 66.6-400 J/cm², respectively, induce a dose-dependent cell death, increase ROS level, disturb mitochondrial functioning and can damage DNA. Thus, the 1265 nm lasers can affect the HCT116 cells through mitochondrial damage. Energy density increase contributes to cell damaging without heating effects.

Recently many interdisciplinary community researchers have focused their efforts on study of the low-level light irradiation effects (photobiomodulation, PBM) as a promising therapeutic technology. Among the priorities a search of new wavelength ranges of laser radiation to enhance the laser prospects in treatment of autoimmune and cancer diseases commonly accompanied by disorders in the antioxidant system of the body. The laser wavelengths within 1265-1270 run corresponds to the maximum oxygen absorption band. Therefore, PBM effects on a model organism within this spectrum range are of particular interest for preclinical research. Here we report comprehensive biomolecular studies of the changes in the BALB/c nude mice skin after an exposure to the continuous laser radiation at the 1270 mu wavelength and energy densities of 0.12 and 1.2 J/cm(2). Such regime induces both local and systemic PBM effects, presumably due to the short-term increase in ROS levels, which in turn activate the cell antioxidative system. (C) 2019 Optical Society of America under the terms of the OSA Open Access Publishing Agreement

In our study, we estimate an effect from chromosome aberrations and genome mutations on changes in microRNA expression profiles in cancer cell lines demonstrating different radiosensitivity. Here, cell viability and microRNA spectrum have been estimated 1, 4, and 24 h after irradiation. MiSeq high-throughput sequencing system (Illumina, San Diego, CA, USA) is employed to perform microRNA spectrum estimation. In the K562 cell line, the number of expressed microRNAs in chromosomes demonstrates a more pronounced variation. An analysis of microRNA effects on signaling pathway activity demonstrates differences in post-transcriptional regulation of the expression of genes included into 40 signaling pathways. In the K562 cell line, microRNA dynamics analyzed for their dependence on chromosome localization show a wider scattering of microRNA expression values for a pair of chromosomes compared to the HL-60 cell line. An analysis of microRNAs expression in the K562 and HL-60 cell lines after irradiation has shown that chromosome abnormalities can affect microRNA expression changes. A study of radiation-induced changes of microRNA expression profiles in the K562 and HL-60 cell lines has revealed a dependence of microRNA expression changes on the number of chromosome aberrations and genome mutations.

In the present work we investigated the molecular nature of the radiosensitizing action of hyperthermia on various cancer cells.