ARTICLE
TITLE

Correction of free radical processes and Mitochondrial dysfunction in rats poisoned by sodium nitrite and tobacco smoke, mildronate preparation

SUMMARY

Introduction. According to the WHO, smoking takes the second place in the list of reasons that cause premature death of people. The interest in clarifying the mechanisms of action on the organism of nitrites and nitrates and the links of the pathogenesis of gemic hypoxia, which thus arises, is due to their widespread use in industry, agriculture and medicine. Therefore, the study of the combined effects of several xenobiotics on the body is feasible and relevant.The aimof the study –to investigate the effectiveness of using antihydroxant Mildronate and its influence on the oxidative processes in the body of rats of different ages infected with sodium nitrite on the background of 45 days of tobacco intoxication.Research methods. Under the conditions of damage to rats of different ages, sodium nitrite on the background of tobacco intoxication was determined in the blood of the content of methemoglobin (MetHb) in reaction with acetone cyanadirin and carboxyhemoglobin (HbCO) in reaction with hexacyanone (III) potassium. The activity of lipoperoxidation processes was assessed by the content of TB? – active products (TB? – AP) in the serum of blood, lungs and myocardium of experimental animals. The evaluation of the functioning of the bioenergetic processes was carried out using the activity of succinate dehydrogenase (SAD), which was studied by the reaction of reduction of potassium ferricyanide, which solution has a yellow color, to colorless ferrocyanide of potassium succinate by the action of EDA and cytochrome oxidase (CO) by the oxidation reaction of dimethyl-n-phenylenediamine.Results and Discussion. It has been established that the defeat of rats of different age groups by sodium nitrite (24 and 72 h before the end of the experiment) on the background of 45 days intoxication with tobacco smoke leads to the activation of free radical oxidation processes, indicating an increase in the content of methemoglobin in the blood of affected animals and TB?-AP in serum of blood, lungs and myocardium after poisoning. At the same time in the blood the content of carboxyhemoglobin increases. In the body, there is a mixed hypoxia (hemitic and circulatory), which leads to disturbances in the functioning of the mitochondrial oxidation chain. The most susceptible to the activity of toxicotoxins were immature animals, and in older animals there was a significant change in the activity of mitochondrial enzymes in the myocardium after the injury, which was more pronounced in comparison with other age groups of rats. In order to correct the revealed violations, a drug of metabolic action with antihypoxant properties of mildronate was used, which positively influenced the activity of lipoperoxidation processes and the activity of mitochondrial enzymes under hypoxia conditions.Conclusions. The obtained results indicate the expediency of inclusion of mildronate in the complex treatment of poisonings of different genesis.

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