Wavelength dependence of oxidative DNA damage induced by UV and visible light
Abstract
DNA damage induced by UV radiation and visible light (290-500 nm) in AS52 Chinese hamster cells was analysed by an alkaline elution assay with specific repair endonucleases. Cells were exposed to extensively filtered monochrome or broad-band radiation. Between 290 and 315 nm, the ratio of base modifications sensitive to Fpg protein (i.e. 8-hydroxyguanine and formamidopyrimidines) and T4 endonuclease V (i.e. cyclobutane pyrimidine dimers) was constant (approximately 1:200), indicating that the direct excitation of DNA is responsible for both types of damage in this range of the spectrum. While the yield of pyrimidine dimers per unit dose continued to decrease exponentially beyond 315 nm, the yield of Fpg-sensitive modifications increased to a second maximum between 400 and 450 nm. The damage spectrum in this wavelength range consisted of only a few other modifications (strand breaks, abasic sites and pyrimidine modifications sensitive to endonuclease III) and is attributed to endogenous photosensitizers that give rise to oxidative DNA damage via singlet oxygen and/or type I reactions. The generation of Fpg-sensitive modifications by visible light was not linear with dose but followed a saturation curve. It is calculated that the exposure of the cells to low doses of solar radiation results in the formation of cyclobutane pyrimidine dimers and Fpg-sensitive modifications in a ratio of 10:1.
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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 [24]
UVB exposure of cellular DNA induces 8-oxodGuo in a yield two to three orders of magnitude lower than CPDs or 6-4PPs.
“The formation of oxidation products, more specifically 8-oxodGuo, is also induced in cellular DNA upon exposure to UVB radiation however in a low yield that is 2-3 orders of magnitude lower than that of either CPDs or 6-4PPs (32).”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions<sup>†</sup> (2012) · cites this paper as [32]
UVA radiation has been shown since the 1970s to induce CPDs in bacteria, mammalian cells and human skin.
“In fact, UVA radiation has been shown since the 1970s, first in bacteria (29) and then in mammalian cells (32,55,(80)(81)(82)(83)(84) and human skin (61,65,(85)(86)(87), to be also able to induce CPDs.”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions<sup>†</sup> (2012) · cites this paper as [32]
The yield of UVA-induced CPDs is larger than that of oxidatively generated lesions such as 8-oxoGua.
“As a striking information, the yield of CPDs was found to be larger than that of oxidatively generated lesions such as 8-oxoGua (32,46,61,88) that were long thought to be the hallmark of UVA genotoxicity, as further discussed below.”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions<sup>†</sup> (2012) · cites this paper as [32]
Oxidized purine bases, most likely 8-oxoGua, are the main UVA-induced oxidation products in UVA-irradiated cells.
“It was found that, oxidized purine bases and most likely 8-oxoGua, are the main UVA-induced oxidation products in UVA-irradiated cells (32,54,115).”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions<sup>†</sup> (2012) · cites this paper as [32]
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Serrentino, M.-E., Catalfo, A., Angelin, A.-R., de Guidi, G., & Sage, E. (2010) · Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis · doi:10.1016/j.mrfmmm.2010.07.011 · Cited by 9 · see citing works
Bennett, M. F., & Cooper, K. D. (2009) · Light-Based Therapies for Skin of Color · doi:10.1007/978-1-84882-328-0_2 · Cited by 2 · see citing works
- Authors
- Kielbassa, C.
- Affiliations
- Johannes Gutenberg University Mainz (DE)
- Corresponding author
- Kielbassa, C
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 1997-04-01
- Volume
- 18
- Issue
- 4
- Pages
- 811-816
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- OpenAlex
- W2045775784
- Cited by
- 616
- References
- 17
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 21 · 2023: 14 · 2022: 22 · 2021: 22 · 2020: 21 · 2019: 24 · 2018: 42 · 2017: 23 · 2016: 38 · 2015: 27 · 2014: 25 · 2013: 32 · 2012: 20
- FWCI
- 5.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Carcinogenesis (publishedVersion)
- PubMed (publishedVersion)
- TNO Repository (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Keywords
- oxidative DNA damage, visible light, ultraviolet radiation, wavelength dependence, cyclobutane pyrimidine dimers, 8-oxoguanine, T4 endonuclease V, endonuclease III, singlet oxygen, endogenous photosensitizers, abasic sites, DNA strand breaks, solar radiation
- MeSH terms
- Animals, DNA Damage, Dose-Response Relationship, Radiation, Cricetinae, Light, Ultraviolet Rays, CHO Cells, Oxidative Stress
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