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ALTERATION OF THE BRAIN AND LIVER TISSUE OF ALBINO RATS WITH LEAD INTOXICATION IN THE DYNAMICS OF THE EXPERIMENT


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Abstract

Introduction. Lead intoxication is one of the most common intoxications with heavy metals. Lead is a global anthropogenic pollutant. The widespread use of lead in human production activities is the main cause of lead pollution of the environment. Lead is capable of the accumulation in the environment and organisms. Central nervous system, detoxification, and excretion systems and hematopoietic system are the most sensitive to lead exposure. The results of experimental modeling of the toxic effect of lead acetate on the organism of albino rats are presented in this paper. Material and methods. Animals with an average mass of 200 g received lead acetate in a dose of 70.5 mg/kg with water. Structural disorders in the brain and liver tissues were determined by methods of review histology. The examination was carried out in two terms - immediately after the end of the exposure and after 9 weeks in a remote post-contact period. Results. The disorder of blood circulation in blood vessels, an increase in the number of stellate macrophages in the Kupffer cells and polynuclear hepatocytes in the liver, and a decrease in the total number of neurons in the brain tissue, development of perivascular edema in the brain tissue and diapedesis of formed blood elements in the perivascular space were revealed as a result of an experiment. There is an increase in the number of neuronophagy acts. In this case, the number of degenerately altered neurons did not differ from the control values. Discussion. Thus, the effect of lead on the body is characterized by a violation of the functions of the circulatory system, the development of a pronounced macrophage response in the liver tissue and death of neurons in the cerebral cortex. Conclusion. The obtained data indicate compensatory processes in the liver tissue of experimental animals to arise under the influence of high doses of lead acetate and persist in a remote post-contact period.


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