Peptide toxins of arthropods are one of the potential sources of bioactive substances. Toxins are able to bind to calcium channels and block them. Ca 2+ ions play an important role in many cell processes, in particular, in apoptosis. In this work, we study the effect of some arthropod toxins on intracellular processes associated with the induction of apoptosis. Synthetic analogs of U 5-scytotoxin-Sth1a, ω-hexatoxin-Hv1a, ω-theraphotoxin-Hhn2a, and μ-agatoxin-Aa1a toxins-inhibitors of calcium L, P, and Q channels and sodium channels were used in the study. Apoptosis was induced by AC-1001 H3 peptide. We study the effect of toxins on the level of apoptosis, ROS, mitochondrial potential, GSH, and ATP in CHO-K1 cells. We show that all the tested toxins are able to dose dependently block the induction of apoptosis triggered by AC-1001 H3 and reduce the level of natural apoptosis in CHO-K1 cells. Cell incubation with apoptosis inducer AC-1001 H3 in the presence and absence of toxins causes an increase in the intracellular concentrations of ROS, ATP, and mitochondrial potential and decreases the GSH concentration. The present study reveals the antiapoptotic effect of a number of arthropod peptide toxins. The toxins studied can represent a novel approach used in the treatment of pathologies associated with the activation of apoptotic mechanisms.

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.

Ischemia-reperfusion injury (IRI) is an irreversible functional and structural injury. Restoration of normal oxygen concentration exacerbates the emergence and development of deadly cells. One of the possible moments of reperfusion damage to cells is an increase in the intracellular concentration of sodium ions. In this article, we study the mu-agatoxin-Aa1a, a modulator of sodium channels, on the processes of IRI cells damage. The toxin was synthesized using an automatic peptide synthesizer. Hypoxia was induced by reducing the content of serum and oxygen in the CHO-K1 culture. The influence of the toxin on the level of apoptosis; intracellular concentration of sodium, calcium, and potassium ions; intracellular pH; totality of reactive oxygen species (ROS), nitric oxide (NO), and ATP; and changes in the mitochondrial potential were studied. The experiments performed show that mu-agatoxin-Aa1a effectively prevents IRI of cells. Toxin reduces the level of apoptosis and prevents a decrease in the intracellular concentration of sodium and calcium ions during IRI. Mu-agatoxin-Aa1a contributes to the maintenance of elevated intracellular pH, reduces the intracellular concentration of ROS, and prevents the decrease in intracellular NO concentration and mitochondrial potential under conditions of reoxygenation/reperfusion. An analysis of experimental data shows that the mu-agatoxin-Aa1a peptide has adaptogenic properties. In the future, this peptide can be used to prevent ischemia/reperfusion tissue damage different genesis.

Ischemic and reperfusion injury is a critical condition, as it is necessary to control cell death and maintain tissue function. Restoration of nutrient and oxygen flow causes secondary damage to ischemic cells and is called reperfusion injury. Reperfusion injury causes, on the one hand, fluctuations in ion concentration inside cells, in particular sodium ions, due to changes in the conductivity of voltage-dependent ion channels, and, on the other hand, activation of the antioxidant system as a response to oxidative stress, in which the key role is given to reactive oxygen species and nitric oxide. Thus, the effect of ion channel inhibitors on the progression of oxidative stress, apoptosis and necrosis during reperfusion is of particular interest. The aim of the study is to examine the impact of sodium channels on oxidative stress under ischemic and reperfusion injury and sodium channel blockers action. Materials and Methods. The authors studied the influence of the synthesized peptide toxin, an inhibitor of voltage-gated sodium channels, under modelled ischemia/reperfusion in CHO-K1 culture on the level of apoptosis, necrosis, and oxidative stress (concentration of reactive oxygen species, nitric oxide, and glutathione) using fluorescent dyes and fluorescence microplate reader. Results. Data obtained indicate a decreased level of apoptosis and necrosis, and a control level of nitric oxide under toxin at a nanomolar concentration. At the same time, the concentrations of reactive oxygen species and glutathione did not change. Thus, the inhibitor toxin acted as a protective agent by preventing a decrease in the nitric oxide concentration, which favorably affected the survival of the cell culture during reperfusion after ischemia.

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.