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KARYOLOGICAL STATUS OF BUCCAL EPITHELIAL CELLS OF MINERS WITH OCCUPATIONAL LUNG PATHOLOGIES


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Abstract

Introduction. Coal dust is the main phlogogenic factor in the development of chronic dust bronchitis in miners. The functional activity of buccal epithelium largely determines the reactivity of the body and modulates the development of the pathological process. Material and methods. 49 miners (mean age of 51.08 ± 0.51 years) with a history of chronic dust bronchitis, 55 miners (mean age of 50.96 ± 0.37 years), without occupational diseases, and 52 men of the control group (mean age of 50.61 ± 3.27 years) were examined with the use of micro-nuclear test to determine the frequency of prevalence rate of buccal epithelial cells with micronuclei, nuclear protrusion “bubble”, “broken egg”, “tongue”, as well as binuclear cells and double-nuclei cells. Results. In miners without occupational diseases, the frequency of the occurrence of cells with micronuclei and double-nuclei was 0.73 ± 0.99‰ and 4.25 ± 3.75‰, for the control group - 0.31 ± 0.53‰ (p = 0.0384) and 2.89±2.76‰ (p = 0.0195), respectively. Significant differences in miners with chronic dust bronchitis regarding the miners without occupational diseases were established on the following nuclear anomalies: the micronuclei (1.69 ± 1.29‰; 0.73 ± 0.,99‰; p = 0.0384), protrusion “bubble” - (2.43 ± 2.08‰; 1.20 ± 1.51 ‰; p = 0,7175), the total frequency of protrusion (3.67±2.88‰; 1.81±2.01‰; p = 0.0001), binucleatedness (5.51 ± 4.28‰; 3.85 ± 4.01‰; p = 0.0129) and double-nuclei - (7.43 ± 4.45‰; 4.25 ± 3.75‰; p < 0.0001). Discussion. No significant associations between nuclear anomalies with work experience and presence of harmful habits (smoking) were found in any of the examined groups. Conclusion. Thus, factors of underground mining production induce clastic and aneugenic effects; worsening hypoxia, related with the deterioration of respiration functions, the influence of inflammatory mediators and impaired redox homeostasis significantly increase the frequency of karyological damage in buccal epithelial cells.


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