Identification of Possible Reactive Oxygen Species Involved in Ultraviolet Radiation-Induced Oxidative DNA Damage
Abstract
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 (1O2) 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 not 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 1O2 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…
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The majority of UV-induced mutations in CS-B cells were G:C→T:A mutations, a signature of 8-oxo-dG-induced mutagenesis.
“Indeed, we found that the majority of UV-induced mutations in CS-B cells were G:C → T:A mutations, a signature of 8-oxo-dG -induced mutagenesis (Fig. 3 F ), which can be caused by direct oxidation of DNA by UV and, more indirectly, by singlet oxygen formation in cells following UV irradiation (24 -26).”
From Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency (2016) · cites this paper as [26]
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Paus, R., Sevilla, A., & Grichnik, J. M. (2023) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2023.09.276 · Cited by 39 · see citing works
Catalase modification as a marker for singlet oxygen.
Lledías, F., & Hansberg, W. (2000) · Methods in Enzymology · doi:10.1016/s0076-6879(00)19013-5 · Cited by 30 · see citing works
Gary, A.-S., & Rochette, P. J. (2020) · Scientific Reports · doi:10.1038/s41598-020-75873-1 · Cited by 30 · see citing works
Aquatic photooxidation of phosphite in the presence of ferric and oxalate ions
Qiu, H.-M., Geng, J.-J., Shen, C.-Y., Ren, H., & Xu, Z.-Y. (2015) · doi:10.1016/j.cej.2015.01.113 · Cited by 28
Klamt, F., Dal-Pizzol, F., Bernard, E. A., & Moreira, J. (2003) · Photochemical and Photobiological Sciences · doi:10.1039/b302785f · Cited by 28 · see citing works
Photodynamic DNA damage mediated by δ-aminolevulinic acid-induced porphyrins
Duez, P., Hanocq, M., & Dubois, J. (2001) · Carcinogenesis · doi:10.1093/carcin/22.5.771 · Cited by 28 · see citing works
Kim, O., Kim, D., Lee, M., Park, S.-H., Yamada, W., Eun, S., & Lee, J. (2021) · Antioxidants · doi:10.3390/antiox10091452 · Cited by 31 · see citing works
“Skin aging caused by UV irradiation is called photoaging, which is characterized by deep wrinkles, pigmentation, dry and rough skin, and loss of moisture and elasticity [16,17].”
BackgroundPiao, M.-J., Lee, N., Chae, S., & Jin, W. H. (2012) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.35.873 · Cited by 27 · see citing works
Sunlight radiation as a villain and hero: 60 years of illuminating research
Powers, J. M., & Murphy, J. E. (2019) · International Journal of Radiation Biology · doi:10.1080/09553002.2019.1627440 · Cited by 29 · see citing works
“The dermatological community has come to a consensus that UVA can penetrate to the dermis to cause photoaging (Lim et al. 2001) as well as DNA damage (Zhang et al. 1997).”
BackgroundShim, J., Park, J.-Y., Lee, M.-G., Kang, H.-H., Lee, T. R., & Shin, D. (2013) · PLoS ONE · doi:10.1371/journal.pone.0067604 · Cited by 26 · see citing works
“Hydrogen peroxide is one of the reactive oxygen species (ROS) associated with UVA-induced cytotoxicity, as described previously [39,40].”
Lee, C.-W., Ko, H.-H., Chai, C., Chen, W.-T., Lin, C.-C., & Yen, F. (2013) · International Journal of Molecular Sciences · doi:10.3390/ijms14023860 · Cited by 25 · see citing works
Photochemical stability of lipoic acid and its impact on skin ageing
Matsugo, S., Bito, T., & Konishi, T. (2011) · Free radical research · doi:10.3109/10715762.2011.587420 · Cited by 25 · see citing works
“characterized ROS induced by UV irradiation by using a set of enzymatic and chemical scavengers, and demonstrated that hydrogen peroxide (H2O2) and hydroxyl radicals (HO) as well as singlet oxygen (O2) are important in UV-induced 8-oxo-7, 8-dihydro-2’-deoxyguanosine (8-oxodGuo) formation following UVA or UVB irradiati…”
BackgroundHorikawa-Miura, M., Matsuda, N., Yoshida, M., Okumura, Y., Mori, T., & Watanabe, M. (2007) · Radiation Research · doi:10.1667/rr0448.1 · Cited by 24 · see citing works
“Both UVB and UVC radiation can generate a spectrum of reactive oxygen species, including hydroxyl radical, singlet oxygen and hydrogen peroxide, in murine cells (26) and in purified calf thymus DNA (27).”
Background
- Authors
- Zhang, X., Rosenstein, B. S., Wang, Y., Lebwohl, M., & Wei, H.
- Affiliations
- City University of New York (US)
- Corresponding author
- Wei, Huachen
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 1997-01
- Volume
- 23
- Issue
- 7
- Pages
- 980-985
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W2089811590
- Cited by
- 216
- References
- 0
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 5 · 2023: 9 · 2022: 8 · 2021: 10 · 2020: 5 · 2019: 11 · 2018: 7 · 2017: 3 · 2016: 7 · 2015: 8 · 2014: 13 · 2013: 9 · 2012: 10
- FWCI
- 2.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r01ca060994-03, 5r01ca061764-04)
- National Cancer Institute (CA61764, CA60994)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- reactive oxygen species, ultraviolet radiation, oxidative DNA damage, 8-oxo-7,8-dihydro-2'-deoxyguanosine, singlet oxygen, hydroxyl radicals, hydrogen peroxide, superoxide, UVA, UV-B radiation, UV-C, sodium azide, catalase, superoxide dismutase, calf thymus DNA, HeLa cells
- MeSH terms
- Catalase, Dimethyl Sulfoxide, DNA Damage, Mannitol, Superoxide Dismutase, Ultraviolet Rays, Free Radical Scavengers, Reactive Oxygen Species, Oxidative Stress, Sodium Azide
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