Introduction. Modern technological processes that generate ultra- and infrasound, electromagnetic, vibration-noise radiation significantly exceed the background effects and inevitably create an unfavorable technogenic load on the human body. A special place is occupied by vibration, primarily associated with such professional groups as mining enterprises, gold and diamond processing plants, aircraft plants, thermal power plants and hydroelectric power plants, and aluminum industry enterprises. Vibration exposure leads to a number of biochemical disorders in the homeostasis system. Mitochondrial dysfunctions are among the leading elements in the hierarchy of pathogenesis of many pathological syndromes and diseases. The aim of the study was an experimental analysis of tissue-specific features of the myocardium, kidneys, liver energy production system activity as well as the enzyme status of rat lymphocytes in relation to the activity of succinate dehydrogenase (SDH) on the background of 7 episodes of local vibration with a frequency of 27-30 Hz for 90 minutes daily before and after protection with succinate-containing antihypoxant "Yantar-cardio" at a dose of 100 mg/kg/day. Materials and methods. The study of the energy-dependent reactions of the native mitochondria of the organs was carried out by the polarographic method using a closed Clark-type membrane electrode. The activity of SDH of rat blood lymphocytes was studied by a modified method of quantitative cytochemical analysis. Results. Functional rearrangement in the respiratory chain (RC) of the mitochondria confirmed the NAD-dependent site's inhibition and activation of the oxidation system of endogenous succinic acid, most pronounced in the myocardial tissue. On the vibration background, the specific SDH activity of lymphocytes (Q) significantly increased by 52%, and the variability (V) - by three times. The use of "Yantar-cardio" limited the growth rate of endogenous respiration of the most significant in the heart (70%, p<0.05), restored oxidative and conjugating activity NAD-dependent link of RC, improve the structure and condition of the cell population of lymphocytes based on their energy status and warned the mismatch of the leading parameters of the population variability of the cellular pool of blood lymphocytes in experimental animals. Conclusions. The intensity of vibration-mediated bioenergetic hypoxia in the form of inhibition of the NAD-dependent link of the respiratory chain and activation of the endogenous succinic acid oxidation system is tissue-specific and is most pronounced in the myocardial tissue. The succinic acid oxidation system is highly sensitive to vibration effects and a pharmacological drug that supports the function of RC under conditions of the stress of the homeostatic functions of tissues involved in the pathological process.

Introduction: The dose-dependent effect of reactive oxygen species (ROS) in tissues in preconditioning (PreC) and oxidative stress, as well as NO-synthase participation in mitochondrial ROS production determined the study aim – to assess the impact of the neuroprotective method of combined preconditioning (CPreC) on free radical reactions (FRRs) in brain in normoxia and in cerebral ischemia, including in NO-synthase blockade. Materials and methods: The intensity of FRR by iron-induced chemiluminescence (CL), the content of lipid peroxidation products and antioxidant enzyme activity were investigated 1 hr (early period) and 48 hrs (delayed period) after CPreC (amtizol and hypobaric hypoxia) in Wistar rat brain. Some animal groups were operated (common carotid artery bilateral ligation) 1 hr and 48 hrs after CPreC, as well as with preliminary introduction of L-NAME and aminoguanidine. Results and discussion: In normoxia, CPreC led to increase the CL maximum level (Fmax) in the delayed PreC period. The amount of thiobarbituric acid reactive products (TBA-RP), activity of superoxide dismutase (SOD) and catalase in mitochondrial fraction of rat brain did not change in comparison with the intact control in both PreC periods. In cerebral ischemia, oxidative stress was observed. The CPreC use before ischemia caused a decrease in CL parameters and TBA-RP in brain, the maintenance of SOD and high catalase activity. NO-synthase inhibitors partially abolished the antioxidant effect of CPreC in ischemia. Conclusion: CPreC had no influence on FRRs in brain tissue in normoxia, but prevented their excessive activation after ischemia, especially in the delayed period. NO-synthase was involved in the CPreC neuroprotection.