Central Asian Journal of Medicine


The aim. A comparative study of activity of multienzyme systems of respiratory chain of mitochondria of liver, which have different sensitivity to hypoxia in conditions of moderate tracheal stenosis. Material and methods. 50 outbred rabbits weighing 2.3-2.5kg were used. Stenosis was created by applying a wide silk ribbon to trachea and narrowing the lumen from 1/3 to 2/3 [8]. Degree of narrowing was determined directly during slaughter of animals, as well as by the nature of the spirogram, clinical signs and by measuring the lumen of stenotic section of trachea relative to original using tracheoscopy. Rabbits were killed by decapitation after 3rd, 7th and 15th day of the experiment and physiological, biochemical and biophysical parameters of blood and liver were determined. Results. Pre incubation at 37°C, NADH-oxidase activity of mitochondria isolated from liver of normal rabbits increases markedly and this high level of activation persists for 6 hours. At the same time, with a 7-day tracheal stenosis, activity of NADH-oxidase undergoes degradation. However, with an increase in duration of tracheal stenosis, activity of NADH-oxidase is restored almost completely to normal level. Thus, disturbances in energy metabolism with moderate tracheal stenosis actually begin in the NAD-dependent section of the respiratory chain and, with an increase in the duration of exposure, extend to the succinate oxidase section. Conclusion. An increase in the activity of poly-enzymatic respiratory chain systems with moderate tracheal stenosis is associated not with an increase in the synthesis of these enzymes, but with an improvement in the access of substrates (NADH, succinate, cytochromes) to the active center of the enzyme system as a result of minor damage to the inner mitochondrial membrane. This is manifested in a violation of the activity of poly-enzymatic systems of the respiratory chain and access of exogenous cytochromes to phospholipids and proteins of mitochondrial membranes, as well as a decrease in their stability when exposed to endogenous and exogenous phospholipases and proteases, leading to disruption of phospholipid-protein and phospholipid-phospholipid interactions of the inner membranes.

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