Abstract
Introduction. The exposure to dust, including chrysotile asbestos, is known to lead to the mobilization of alveolar macrophages, accompanied by the activation of free radical oxidation and the release of mediators stimulating fibroblast proliferation and collagen synthesis. Material and methods. Thirty outbred male rats were divided into two groups: 1 - control with a period of 4 months (n = 15), the 2-experienced group subjected to 4-month seed with chrysotile asbestos dust (n = 15). Under ether anesthesia, animals of the experimental group once were installed intratracheally in the respiratory tract using a syringe 1.0 ml of the sterile saline solution containing a suspension (50 mg) of chrysotile dust - asbestos. Then, the animals were killed, their bronchial washes, centrifuged, smears from the sediment, were subsequently visualized with a microscope. Fat metabolism was assessed by the content of phospholipids in the cell, according to G.A. Merkulov. Determination of hydroxyproline in the pulmonary homogenate. The statistical differences between the two groups were assessed with the Student’s t-test. Data were expressed as mean ± SE. Probability values of p <0.05 were considered significant. Results. The chronic exposure to chrysotile asbestos dust with a period of 4 months was found to causes a decrease in the activity of phagocytic cells and an increase in the destructive forms of alveolar macrophages in bronchoalveolar washes, excessive accumulation of phospholipids and an increase in oxyproline. Pneumofibrosis develops due to the cytotoxic and membrane-damaging effect of chrysotile asbestos dust. Conclusion. Thus, chrysotile asbestos dust from the Zhitikarinsky site, attributed to nanoparticles and multicomponent in chemical composition, has a cytotoxic effect, accompanied by activation of phagocytic pulmonary membrane and membrane-destructive changes in cells with accumulation of phospholipids.