[THE STRUCTURE AND RISK OF CHRONIC MORBIDITY IN SOME VILLAGES OF THE UPPER IMERETI REGION OF WEST GEORGIA AND THEIR MOLECULAR AND CYTOGENETIC MARKERS].

The purpose of our study was to identify the nature of the cause-effect relationship between the risks of developing of Chronic Obstructive Pulmonary Disease (COPD) and Cardio-vascular Disease (CVD) in patients residing in the villages of Chiatura district, characterized by varying degrees of environmental stress. The residents (n=400) of the Chiatura district living in the villages, Khreiti, Perevisa and Rgani were examined. The villages are characterized by different degrees of ecological tension (the villages differ both in their remoteness from sources of environmental pollution - manganese mining quarries and the scale of its extraction, which allows them to rank according to the degree of environmental tension: Khreiti - low, Perevis - medium, Rgani - high). In the patients the blood general redox balance and genetic parameters (the number of micronuclei in the scrapings of the oral mucosa) were studied. In the zone of moderate environmental stress (the village of Perevisa), a significant increase in the indicator of the total antiradical activity of blood plasma and an increase in the frequency of micronucleated buccal cells were revealed in comparison with the zone of low environmental stress (the village of Khreiti). In residents of the village of Rgani, characterized by the highest level of pollution, the indicator of the total antiradical activity of blood plasma decreases sharply, the number of micronuclei decreases, the presence of various types of damage to the nucleus is noted, which is characteristic of intensive apoptosis. Under the conditions of moderate air pollution, observed mobilization of protective anti-radical and replication mechanisms in the body are aimed at preserving the stability of the somatic cell genome. Identified oxidative stress can also act as mediators of secondary alteration and the development of the inflammatory process in the circulatory bed, resulting in an increased risk of arterial hypertension (AH) against the background of a relatively high risk of chronic nonspecific obstructive pulmonary diseases (COPD). High level of environmental pollution contributes to the development of permanent intense oxidative stress in the affected tissues of the respiratory tract. That contributes to the development of predominantly nonreparable changes in the cell genome, apoptosis and intensification of secondary oxidative stress, which, under conditions of depletion of antiradical protection, causes preferential defeat of the microenvironment of apoptotic cells, the development of local effects, reflected in a sharp increase in the risk of COPD.