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PEROXIDATION OF BLOOD LIPIDS IN THE CONDITIONS OF APPLICATION OF INDIVIDUAL RESPIRATORY PROTECTION EQUIPMENT


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Abstract

Introduction. The category of important, but little-studied environmental factors, is the additional respiratory resistance, which is the main factor limiting human performance in the means of individual respiratory protection. Changes in the body that have not been sufficiently studied under conditions of additional respiratory resistance include changes in lipid peroxidation and antioxidant protection. The purpose of this study was to study changes in blood lipid peroxidation using additional respiratory resistance. Material and methods. The study was conducted on practically healthy subjects of both sexes (78 people), aged from 20 to 36 years. To simulate the conditions of use of personal protective equipment for respiratory organs, inspiratory resistive respiratory loads of 20% of the maximum intraoral pressure were used for the Muller test. The duration of the resistive loads amounted to 3 or 10 minutes. The processes of lipid peroxidation were assessed by changes in the level of malonic dialdehyde, the concentration of free fatty acids, and the dynamics of plasma hydroperoxides. The activity of the antioxidant system was determined by the dynamics of the index of total antioxidant activity, plasma catalase activity. Measurement of serotonin, adrenaline and noradrenaline concentrations in plasma was carried out by the fluorimetric method. Results. The indices of blood lipid peroxidation are most affected by the duration of use of respiratory protective equipment. Three-minute respiration in the means of individual respiratory protection significantly changed the processes of peroxidation of blood lipids in the direction of inhibition. In particular, there was decreased the concentration of malonic dialdehyde decreased (p <0.01); concentration of free fatty acids (p <0.001), and activity of lipid hydroperoxides (p <0.0001). Under a ten-minute use of personal respiratory protection, the processes of blood lipid peroxidation almost did not change: the content of lipid hydroperoxides and malondialdehyde remained unchanged (p> 0.05) from the initial level. Conclusion. The antioxidant effects of the values of increased resistance to breathing used by us indicate to the absence of hypoxic stimulation under the action of moderate resistive loads, and resistive stimulation of antioxidant mechanisms. We assume that during the action of resistive respiratory loads, the metabolic function of the lungs is activated, which is associated with increased resorptive processes in the pulmonary vessels, which leads to an enhanced release of biologically active substances from the lungs with antioxidant activity. Enhancement of the absorption of endogenous antioxidants against the background of resistive respiratory loads is a protective response against lipid peroxidation.


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