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 ± 1.57^a	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 ± 7.01^b	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).