The Cellular Response to Oxidatively Induced DNA Damage and Polymorphism of Some DNA Repair Genes Associated with Clinicopathological Features of Bladder Cancer
Table 4
The cellular response to DNA damage in the groups of BC patients, elderly people, and individuals with chronic inflammatory diseases.
Features under study
BC patients ( = 40)
Individuals older than 60 years ( = 15)
Individuals with chronic inflammations ( = 15)
Average age (mean ± SE)
69.55 ± 1.57a
62.8 ± 0.74
48.87 ± 2.86
Sex ratio females/males (% of males)
6/34 (85)
4/11 (73.33)
7/8 (53.33)
Smokers/nonsmokers (% of smokers)
5/35 (89)
6/9 (60)
2/13 (13.33)
Basal DNA damage (a.u.) at 180 min
11.38 ± 1.09
9.93 ± 2.61
6.0 ± 1.32
H2O2-induced DNA damage (a.u.) at 0 min
117.13 ± 7.01b
89.33 ± 11.55
92.47 ± 7.97
Residual level of H2O2-induced DNA damage (a.u.) at 180 min
17.7 ± 1.59
18.2 ± 4.21
12.77 ± 3.03
DNA repair efficiency for 30 min incubation
65.24 ± 2.08
69.91 ± 3.82
66.23 ± 4.03
DNA repair efficiency for 180 min incubation
84.25 ± 1.33
81.27 ± 3.27
84.72 ± 3.22
Significant differences concerning age were revealed between BC patients and elderly persons ( = 0.0004) and between BC patients and individuals with chronic inflammatory diseases ( = 0.0001). bSignificant differences concerning the initial level of H2O2-induced DNA damage were observed between BC patients and elderly persons ( = 0.05) and between those and individuals with inflammations ( = 0.027).