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 

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.

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 this paper, we have studied the role of chromosomal abnormalities in the expression of small nucleolar RNAs (snoRNAs) of radioresistant (K562) and radiosensitive (HL-60) leukemia cell line. Cells were exposed to an X-ray dose of 4 Gy. SnoRNA expression was investigated using NGS sequencing. The distribution of expressed snoRNAs on chromosomes has been found to be different for two cell lines. The most significant differences in the expression of snoRNAs were found in the K562 cell line based on the analysis of the dynamics of log2fc values. The type of clustering, the number and type of snoRNAs slightly differed in the chromosomes with trisomy and monosomy and had a pronounced difference in pairs with marker chromosomes in both cell lines. In this study, we have demonstrated that chromosomal abnormalities alter the expression of snoRNA after irradiation. Trisomies and monosomies do not have such a noticeable effect on the expression of snoRNAs as the presence of marker chromosomes.

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.