Accumulation of DNA damage may play a significant role in the aetiology of the ageing process. Although genomic lesions increase the risk of cancer, many elderly individuals do not suffer from neoplasia in spite of their late age. We aimed to evaluate the rate of genome integrity impairment among elderly subjects without recorded chronic or inflammatory diseases and malignancies. Thirty-one generally healthy elderly subjects (age 69.3 +/- 3.7 years) were studied. Subjects matched control subjects by gender and lifestyle factors. Frequencies of structural chromosome aberrations and translocations applying fluorescence in situ hybridization chromosome painting probes, levels of primary DNA damage and oxidative lesions cleaved by hOGG1 enzyme using alkaline and hOGG1-modified comet assay were recorded in peripheral blood leukocytes. Also, susceptibility of the genome to H(2)O(2)-induced damage as a marker of antioxidative status was evaluated. Translocation yields and rates of chromatid breaks and acentric fragments were significantly higher among elderly subjects. Furthermore, a significant increase in the level of primary genome lesions and hOGG1-sensitive sites in DNA was detected, while the results of the comet assay following H(2)O(2) pre-treatment suggested decreased levels of antioxidant protection in leukocytes. The results obtained may indicate that accumulation of genome damage observed in leukocytes of elderly subjects as surrogate cells is intertwined with the ageing process. Taking this into consideration with the medical records of the study subjects, the results support other authors' findings that the accumulation of basal genome damage might not inevitably trigger the mechanism that enforces induced development of neoplasia.