ULTRASTRUCTURAL BASIS OF CARDIOTOXIC ACTION OF LEAD ACETATE ON CARDIAC MORPHOGENESIS

Dovgal G. V., Shevchenko I. V.

MORPHOLOGY

Scentific article

In modern society, changes in the environment that arise under the influence of anthropogenic factors, an increase in the number of salts of heavy metals, which are teratogens and can provoke disorders in the development of organs, are the object of interest. One such compound is lead acetate. Lead acetate has a high polytropic toxicity. Influence on physiology, organ morphogenesis and metabolic parameters was studied in experimental studies and recorded in patients with acute intoxication. The heart and the vascular system are sensitive to the effects of lead compounds, during the prenatal and postnatal period. Many mechanisms have been proposed to explain lead-induced hypertension, including changes in calcium and sodium metabolism, disturbances in the functioning of the renin-angiotensin system, involvement of the sympathetic nervous system, and increased sensitivity to other compounds. At the biochemical level, toxicity is due to a disturbance in the oxidation-reduction equilibrium, hyperproduction of free radicals, and damage to endogenous antioxidant systems. Investigation of the influence on the development of one or another organ in the embryo after exposure to the mother’s body with such teratogens as, for example, lead acetate is far from complete. In this aspect, comparative embryology and its experimental methods of investigation become important. The identification of the primary signs of cardiotoxicity is not an easy task. Thus, it is known from literary sources that the earliest ultrastructure imines are affected by cardiomyocyte damage are changes in mitochondria. In this case, the morphology of the organelle can have significant variability, and some of the forms have a connection with the mechanism of damage. So, first a reduction in the electron density of the matrix is recorded, then the matrix swelling occurs. The edema of the cyst ends with their destruction, which explains the cause of the energy deficit in cardiomyopathy. The decrease in the density of myofibrils in our own studies was detected already on the first day of the exposure of lead acetate. Changes in the density of myofibrils on day 7 were not detected, indicating a certain stability of these protein structures. At the same time, the length of sarcomeres was reduced. These changes should not be considered as a manifestation of the recovery process, since a significant number of myofibers have suffered damage. The general conclusion is an increase in the destructive changes in cardiomyocytes during the exposure of lead acetate. The manifestation of cardiotoxic action of lead acetate is edema of cardiomyocytes, destructive changes in mitochondria and reduction of myofibrils. Ultrastructural disorders are a consequence of the acute toxic effects of lead acetate.

lead acetate, heart, myocardium, matrix, myofibril, cardiomyocytes, sarcomere, kristi, cardiotoxic effect of lead acetate

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«Bulletin of problems biology and medicine» Issue 2 (144), 2018 year, 306-310 pages, index UDK 616.447-089.87

10.29254/2077-4214-2018-2-144-306-310