NDT Advance Access published online on November 4, 2009
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp575
Oxidative DNA damage in chronic renal failure patients
1 Grup de Mutagènesi, Departament de Genètica i de Microbiologia, Edifici Cn, Universitat Autònoma de Barcelona, 08193 Bellaterra, Cerdanyola del Vallès, Spain 2 Fundació Puigvert, Barcelona, Spain 3 CIBER Epidemiología y Salud Pública, ISCIII, Spain
Correspondence and offprint requests to: Ricard Marcos; E-mail: ricard.marcos{at}uab.es
| Abstract |
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Background: Chronic renal failure (CRF) patients present a high incidence of cardiovascular pathologies and cancer. This has been attributed to the existence of genomic instability in these patients, and consequently they should present elevated levels of genetic damage.
Methods: To determine the background levels of genetic damage and its specific levels of oxidative damage, a large population of 253 CRF patients (77 in dialysis) was analysed using the comet assay. The percentage of DNA in the tail was used as a measure of basal genetic damage. In addition, the use of endo III and FPG enzymes allowed us to determine the levels of specific oxidative damage in DNA bases.
Results: This is the first study that uses endo III and FPG enzymes to measure oxidative damage in CRF patients. Overall genetic damage, as well as specific oxidative damage, was higher in dialysis patients than in the CRF patients with different stages of uraemic state; genetic damage increased when serum creatinine levels increased. Genomic damage in dialysis patients decreased in those patients submitted to dialysis for a long time.
Conclusions: Genetic damage increases when renal function decreases, being maximum in haemodialysis patients. Although part of the observed damage can be attributed to the uraemic state itself, other individual genetic factors can influence a state of genomic instability responsible for the observed genomic damage.
Keywords: comet assay; CRF; haemodialysis treatment; oxidative damage; uraemic state
Received for publication: 9. 3.09
Revision received 29. 9.09.
Accepted in revised form: 2.10.09