Динаміка змін маркерів біоенергетичних процесів та цитолізу у щурів після ураження нітритом натрію на тлі тютюнової інтоксикації

Abstract

В експерименті на білих щурах різних вікових груп, отруєних натрію нітритом на тлі 15 денної інтоксикації тютюновим димом, встановлено пригнічення активності маркерних ферментів мітохондріального окиснення – сукцинатдегідрогенази та цитохромоксидази — у печінці, легенях та міокарді тварин. Одночасне ураження обома токсикантами поглиблює розвиток мембранодеструктивних процесів, про що свідчить зростання активності амінотрансфераз у сироватці крові після отруєння та зниження у досліджуваних органах. Найбільш чутливими до дії натрію нітриту на тлі ураження тютюновим димом виявились статевонезрілі тварини; В эксперименте на белых крысах разных возрастных групп, отравленных натрия нитритом на фоне 15 дневной интоксикации табачным дымом, установлено угнетение активности маркерных ферментов митохондриального окисления – сукцинатдегидрогеназы и цитохромоксидазы – в печени, легких и миокарде животных. Одновременное поражение обоими токсикантами усугубляет развитие мембранодеструктивных процессов, о чем свидетельствует увеличение активности аминотрансфераз в сыворотке крови после поражения в исследуемых органах. Наиболее чувствительными к действию натрия нитрита на фоне поражения табачным дымом оказались половонезрелые животные; Smoking is a risk factor serves more than 20 diseases, which make up almost 75% in the structure of causes of mortality. Smoking has a negative impact not only on individuals who smoke themselves, the so-called «active» smokers, but also for other people who inhale tobacco smoke from the environment. One risk factor is excessive food intake, which is dominated by products that underwent processing nitrate fertilizers. Poisoning these compounds leads to hemic hypoxia, caused by the excessive formation of methemoglobin and activation of free radical processes in the organism. Activation of free radical oxidation and the development of hypoxia is one of the most important causes of metabolic disorders in conditions of toxicants poisoning of various origins. Mitochondrial dysfunction associated with the processes of oxidative phosphorylation, mitochondrial structural integrity and identity of their genetic information system, arising under conditions of oxidative stress in diseases caused by metabolic disorders. Objective. Explore the power supply system and markers of cytolysis cells in rats of different ages, poisoned by sodium nitrite on the background of 15-day tobacco intoxication. Methods. Experiments conducted on white male rats of three age categories: immature, mature and old rats. Rats of experimental groups for 15 days exposed to tobacco smoke. The test animals were divided into 3 groups. One of them for 24 hours before the end of the experiment were injected sodium nitrite at a dose of 45 mg/kg, the second — sodium nitrite was administered 72 hours before euthanasia. The third group of rats subjected to the toxic effects of tobacco smoke only. Tobacco smoke formed by burning cigarettes 6 «Prima silver (blue)» and (containing 0.6 mg of nicotine and tar 8 mg), through openings in the chamber was fed into it. After 15 days from the beginning of the defeat of animals tobacco smoke deduced from the experiment by euthanasia tiopental under anesthesia. Assessment of functioning bioenergy processes performed by succinatedehydrogenase and cytochromeoxidase activity, cytolysis cells after defeat toxicants — in aminotransferase activity. Statistical analysis of the data was performed using the «STATISTICA 6,0» using parametric Student’s t test and the nonparametric Wilcoxon test for related samples. Results. Poisoning rats of all ages tobacco smoke for 15 days resulted in a slight decrease in activity of SDG in the liver, lungs and the myocardium. Significant changes were noted. After the destruction of animals sodium nitrite intoxication on the background of the tobacco enzyme activity suffered a possible downgrade. Most sensitive to the simultaneous action of two toxins appeared immature rats. After the destruction of rats sodium nitrite and tobacco smoke cytochromeoxidase activity experienced a sharp inhibition in rat organs-term all categories compared to the intact group. We observed significant increase of ALT activity in serum immature rats in all experimental groups. The possible increase in ALT activity in serum of senile animals observed in the groups of animals that once poisoned two toxicants. In the liver, lungs and the myocardium of rats after poisoning with both toxicants decreased ALT activity. In parallel, we studied the activity of AST in different tissues of experimental rats of all ages. Serum AST activity highest value observed in immature rats in the last period of the study. In the organs of experimental animals was noted reduced activity of the enzyme. After the defeat of the rat tobacco smoke and sodium nitrite marked cytolysis of all investigated cells, as evidenced by decreased activity of aminotransferases in the liver, lungs and heart of poisoned animals and increase the activity of both enzymes in serum. Conclusions. Poisoning rats of different ages sodium nitrite intoxication on the background of tobacco membrane- destructive accompanied by development processes in the body, and as a result — inhibition processes of tissue respiration, particularly the activity of mitochondrial enzyme — succinate dehydrogenase and cytochrome oxidase.