Identification of possible reactive oxygen species involved in ultraviolet radiation-induced oxidative DNA damage
Identification of possible reactive oxygen species involved in ultraviolet radiation-induced oxidative DNA damage
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DOI:
10.1016/s0891-5849(97)00126-3
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发表时间:
1997-01-01
影响因子:
7.4
通讯作者:
Wei, HC
中科院分区:
文献类型:
--
作者:
Zhang, XS;Rosenstein, BS;Wei, HC
We have previously demonstrated that each region of the ultraviolet (UV) spectrum (UVA, UVB, and UVC) induces the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) in purified calf thymus DNA and HeLa cells in a fluence-dependent manner. In the present study, we further characterize the possible reactive oxygen species (ROS) that are involved in the induction of 8-oxodGuo by UV radiation. Sodium azide, a singlet oxygen (O-1(2)) scavenger though its quenching effect on HO . was also reported, inhibited 8-oxodGuo production in calf thymus DNA exposed to UVA, UVB, or UVC in a concentration-dependent fashion with maximal quenching effect of over 90% at a concentration of 10 mM. Catalase, at a concentration of 50 U/ml, reduced the yields of UVA-and UVB-induced 8-oxodGuo formation by approximately 50%, but had little effect on UVC-induced 8-oxodGuo production. In contrast, 50 U/ml of superoxide dismutase (SOD) did nor affect induction of 8-oxodGuo by any portion of the UV spectrum. Hydroxyl radical (HO .) scavengers mannitol and dimethylsulfoxide (DMSO) moderately reduced the levels of 8-oxodGuo induced by UVA and UVB, but not those by UVC. instead, mannitol and DMSO enhanced the formation of 8-oxodGuo induced by UVC. These results suggest that certain types of ROS are involved in UV-induced 8-oxodGuo formation with O-1(2) playing the predominant role throughout the UV spectrum. Except for UVC, other ROS such as hydrogen peroxide (H2O2) and HO . may also be involved in UVA- and UVB-induced oxidative DNA damage. Superoxide anion appears not to participate in UV-induced oxidation of guanosine in calf thymus DNA, as SOD did not display any quenching effects. (C) 1997 Elsevier Science Inc.