Spontaneous DNA repair in human peripheral blood mononuclear cells.
DNA molecules are constantly damaged during mitosis and by oxygen-free radicals produced by either cellular metabolism or by external factors. Populations at risk include patients with cancer-prone disease, patients under enhanced oxidative stress, and those treated with immunosuppressive/cytotoxic therapy. The DNA repair process is crucial in maintaining the genomal DNA integrity. The aim of this study was to evaluate spontaneous DNA repair capacity of peripheral blood mononuclear cells (PBMC) from normal blood donors. PBMC DNA repair ability represents DNA repair by other tissues as well. It is shown in the present study that in vitro incorporation of [3H]thymidine in non-stimulated PBMC expresses the ability of the cells to repair DNA damage. This method was validated by double-stranded DNA measurements. Both catalase and Fe2+ increased DNA repair, the former by preventing re-breakage of newly repaired DNA and the latter by introducing additional DNA damage, which enhanced DNA repair. Better understanding of DNA repair processes will enable to minimize DNA damage induced by oxidative stress.
Ori
Yaacov
Y
Department of Nephrology and Hypertension, Rabin Medical Center, Petah-Tikva 49372, Israel.
Herman
Michal
M
Weinstein
Talia
T
Chagnac
Avry
A
Zevin
Dina
D
Milo
Gai
G
Gafter
Uzi
U
Malachi
Tsipora
T
D003561:Cytarabine / Q000494:pharmacology; D004260:DNA Repair / Q000187:drug effects; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007501:Iron / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D013050:Spectrometry, Fluorescence
D003561:Cytarabine; D006861:Hydrogen Peroxide; D007501:Iron; D004121:Dimethyl Sulfoxide