Abstract
Materials and Methods: The main goal of this study was to investigate the effects of endogenous nitric oxide on mitochondrial respiration and to study the effects of blue (442 nm) and green (532 nm) low-power radiation on mitochondrial respiration in experimental endotoxic shock. We used a model of experimental endotoxic shock produced by intraperitoneal injection of lipopolysaccharide B. Results: Low-power laser radiation has an appreciable effect on the rate of mitochondrial respiration in states of 3 and 4, both in normal and in endotoxic shock. The result of blue laser radiation (442 nm) was an increase of mitochondrial respiratory rate V3 in the control group by 12% at dose of 6 J/cm2. Increasing the irradiation dose lead to gradual decrease in rate V3. In the case of green laser (532 nm), statistically significant deviations from control in the rate V3 is not revealed. The greatest increase in respiratory rate in state of V3 (about 30%) was observed in LPS-treated animals at dose of 6 J/cm2 (442 nm). Oxygen consumption rate in the state of 4 irradiation at dose of 10 J/cm2 increased compared to the control all sources of radiation. In an experimental endotoxic shock rate of oxygen consumption by mitochondria V4 also increased (approximately 40%) for all sources, but this effect was more pronounced than in the control group. To evaluate the mitochondria membrane potential in experimental endotoxic shock a JC-1 fluorescent probe was applied. It was found that statistically significant difference (approx. 10%) exists in the mitochondria membrane potential of in LPS-treated and untreated rats. This phenomenon could be due to the membrane damage in endotoxic shock development. Conclusion: Study of the effect of laser radiation on mitochondrial respiration showed that in experiments using blue laser (442 nm), an increase rate V3 and V4, which can be attributed to the destruction of nitrosyl complexes of the respiratory chain. This tendency was more pronounced in an experimental endotoxic shock.
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