In case of any accidental mass exposure and particularly in cases of radiation contamination, there is a need to estimate possible effects in a short time. The best known, gold standard, accurate and associated to cancer risk increase proofed measurement of absorbed dose via classic cytogenetics is unfortunately laborious and time consuming. The aim of our human monitoring studies performed on subjects from various cities and countries was to investigate if exposures to genotoxic agents, environmental, occupational, diagnostic or therapeutic can cause a detectable increase risk. Exposures to ionizing radiation, pesticides, mercury ions, benzene related compounds have significantly elevated levels of cytogenetic damage. The 25 years follow up studies revealed significantly increased risk of cancer in the group of subjects characterized by the highest levels of the detected chromosomal damage. Results of DNA repair competence assay, with a use of challenging dose of X-rays and the detection of induced DNA damage by the SCGE assay, have correlated to levels of induced chromosome damage detected by classic and FISH cytogenetic methods. Results from studies on the influence of occupational exposure to environmental PAHs, on the efficiency of the radiation induced DNA damage’s repair, have shown a strong variability between donors and significant decrease of the DNA repair efficiency in exposed subjects, that was strongly differentiated between groups stratified first according to various genotypes for genes, encoding enzymes involved in the process of bio-transformation (CYP1A1(Ile/Val), GSTM1, NAT2) or DNA repair (EPHX4 or XRCC1)1 and then to levels of exposures. Results of our studies in various groups of (prostate or colon cancers or thyroid diseases) patients have also shown the higher levels of chromosome aberrations frequencies and associated significant reduction of cellular DNA repair efficacy in comparison to healthy subjects groups. Thyroid patients were examined first after low diagnostic 131 one, and another time five weeks after medical treatments with higher doses. Strong inter individual variability was observed. Preliminary study of polymorphisms XRCC1 and XRCC3 genes encoding enzymes involved in the repair process, confirmed strong influence of genes of the DNA damage induced by IR and stepped up levels of biomarkers, the predictor of cancer risk. Our results demonstrate also that the DNA repair competence biomarker (RCB), fast and inexpensive, can reliably detects an influence of ontogenetic or exogenous factors on biological effects, which via alteration of the DNA repair processes can rise levels of chromosome aberrations and result in increased health risk. That knowledge might be key factor in stratification of the population at risk, or in predicting beneficial range for high dose therapeutic procedures.


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  • Received: 09 May 2012
  • Accepted: 09 May 2012
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