TY - JOUR
T1 - Genotoxicity and DNA repair processes of zinc oxide nanoparticles
AU - Demir, Eşref
AU - Creus, Amadeu
AU - Marcos, Ricard
PY - 2014/1/1
Y1 - 2014/1/1
N2 - Copyright © 2014 Taylor & Francis Group, LLC. Two different sizes of zinc oxide nanoparticles (ZnO NP, ≤35 nm and 50-80 nm) were tested in the human lymphoblastoid cell line TK6 to increase our knowledge on their genotoxic potential. The comet assay was the system used, and the results obtained showed that the highest concentration tested (100 μg/ml) for the two selected compounds was genotoxic. The percent DNA in tail obtained after treatment with ZnO NP (≤35 nm) was significantly higher than that of ZnO NP (50-80 nm) at all concentrations tested. To investigate the nature of the induced genotoxic damage, specific enzymes recognizing oxidized DNA bases were used. Treatments with endonuclease III (Endo III) and formamidopyrimidine DNA glycosylase (FPG) demonstrated that only ZnO NP (50-80 nm) were able to induce significant levels of net oxidative DNA damage. Further DNA repair kinetics studies revealed that DNA damage initially induced was removed in approximately 5 h. DNA damage induced by ZnO NP was repaired more slowly than damage following microparticulated ZnO exposure. No marked differences in repair kinetics of both forms of ZnO NP were observed. Evidence indicates that a high proportion of DNA damage induced by ZnO NP (50-80 nm) correlated with induction of oxidative damage, and that both forms of ZnO NP interfere with mechanisms involved in DNA damage repair.
AB - Copyright © 2014 Taylor & Francis Group, LLC. Two different sizes of zinc oxide nanoparticles (ZnO NP, ≤35 nm and 50-80 nm) were tested in the human lymphoblastoid cell line TK6 to increase our knowledge on their genotoxic potential. The comet assay was the system used, and the results obtained showed that the highest concentration tested (100 μg/ml) for the two selected compounds was genotoxic. The percent DNA in tail obtained after treatment with ZnO NP (≤35 nm) was significantly higher than that of ZnO NP (50-80 nm) at all concentrations tested. To investigate the nature of the induced genotoxic damage, specific enzymes recognizing oxidized DNA bases were used. Treatments with endonuclease III (Endo III) and formamidopyrimidine DNA glycosylase (FPG) demonstrated that only ZnO NP (50-80 nm) were able to induce significant levels of net oxidative DNA damage. Further DNA repair kinetics studies revealed that DNA damage initially induced was removed in approximately 5 h. DNA damage induced by ZnO NP was repaired more slowly than damage following microparticulated ZnO exposure. No marked differences in repair kinetics of both forms of ZnO NP were observed. Evidence indicates that a high proportion of DNA damage induced by ZnO NP (50-80 nm) correlated with induction of oxidative damage, and that both forms of ZnO NP interfere with mechanisms involved in DNA damage repair.
U2 - 10.1080/15287394.2014.935540
DO - 10.1080/15287394.2014.935540
M3 - Article
SN - 1528-7394
VL - 77
SP - 1292
EP - 1303
JO - Journal of Toxicology and Environmental Health - Part A: Current Issues
JF - Journal of Toxicology and Environmental Health - Part A: Current Issues
ER -