Cytogenetic effects of excessive radon exposure depending on the individual dosage of active ribosomal genes

Abstract

Background. Maintaining radon safety is one of the most critical challenges in modern ecology and genetic toxicology. Radon (222Rn) and its decay daughter products (218Po, 214Po, 214Pb and 214Bi) can interact with biological tissues and induce DNA damage. Because transcribed copies rDNA are necessary for DNA damage repair, we examined whether genomic dosages of active ribosomal genes modulate the genotoxic effects of exposure to high doses of radon.
 Materials and methods. Chromosome aberration assay in peripheral blood lymphocytes was performed in pupils of the boarding school of Tashtagol (Kemerovo region, Russia) with long-term resident exposure to radon (n = 345) and in childrenof the Kemerovo Region living in radiation-safe conditions (n = 233). The dose of active (transcription-capable) ribosomal gene (AcRG) in the studied groups has been analyzed using Ag-NORS staining regions of chromosomes and cytogenetic semi-quantitative evaluation method.
 Results. A statistically significant increase in the level of chromosome aberrations in exposure group has been revealed compared with the children of the Kemerovo Region living in radiation-safe conditions (p = 0.00001). It was found that the level of chromosomal abnormalities in Tashtagol’s children was higher in medium-dose carriers of AcRG compared to owners of a low dose (4.27 ± 0.22% vs. 3.24 ± 0.29%, p = 0.003). Perhaps the low level of chromosomal aberrations in children with low-dose AcRG is associated with an increase in cell death from damaged DNA under genotoxic exposure to radon.
 Conclusion. The obtained results testify to the significant contribution of the individual characteristics of ribosomal genes in the formation of genotoxic effects of exposure to high doses of radon.