UVA1 Induces Cyclobutane Pyrimidine Dimers but Not 6-4 Photoproducts in Human Skin In Vivo

Tewari, Angela; Sarkany, Robert; Young, Antony R.

doi:10.1038/jid.2011.283

Cited by 125 publications

(111 citation statements)

References 46 publications

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“…C are generated (but not 6-4PPs) in fibroblasts, keratinocytes, melanocytes, and human skin (Mouret et al 2006(Mouret et al , 2008(Mouret et al , 2011. Histoimmunochemical measurements confirmed the presence of CPDs in the epidermis, whereas 6-4PPs were not detected (Tewari et al 2012). Interestingly UVB-induced CPDs were predominantly located at the basal level of the epidermis in contrast to CPDs, whose concentration decreases as the depth increases (Tewari et al 2012).…”

Section: Uva-mediated Formation Of Cyclobutane Pyrimidine Dimersmentioning

confidence: 81%

“…Histoimmunochemical measurements confirmed the presence of CPDs in the epidermis, whereas 6-4PPs were not detected (Tewari et al 2012). Interestingly UVB-induced CPDs were predominantly located at the basal level of the epidermis in contrast to CPDs, whose concentration decreases as the depth increases (Tewari et al 2012). The mechanism of formation of UVA-induced CPDs, which shows features of triple -triplet energy transfer with respect to the distribution of bipyrimidine photoproducts, has remained under debate until recently.…”

Section: Uva-mediated Formation Of Cyclobutane Pyrimidine Dimersmentioning

confidence: 91%

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DNA Base Damage by Reactive Oxygen Species, Oxidizing Agents, and UV Radiation

Cadet

Wagner

2013

Cold Spring Harbor Perspectives in Biology

720

510

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Emphasis has been placed in this article dedicated to DNA damage on recent aspects of the formation and measurement of oxidatively generated damage in cellular DNA in order to provide a comprehensive and updated survey. This includes single pyrimidine and purine base lesions, intrastrand cross-links, purine 5 0 ,8-cyclonucleosides, DNA-protein adducts and interstrand cross-links formed by the reactions of either the nucleobases or the 2-deoxyribose moiety with the hydroxyl radical, one-electron oxidants, singlet oxygen, and hypochlorous acid. In addition, recent information concerning the mechanisms of formation, individual measurement, and repair-rate assessment of bipyrimidine photoproducts in isolated cells and human skin upon exposure to UVB radiation, UVA photons, or solar simulated light is critically reviewed.I n this article, we emphasize recent developments in the formation of damage to cellular DNA mediated by reactive oxygen species (ROS) and oxidizing agents, including singlet oxygen, the hydroxyl radical ( † OH), one-electron oxidants, hypochlorous acid (HOCl), and ten-eleven translocation (TET) oxygenases involved in epigenetic regulation. These advances have been possible because of the development of sensitive and powerful high-performance liquid chromatography-mass spectrometry (HPLC-MS)/ mass spectrometry (MS) methods allowing one to revise previously reported data obtained using methods such as gas chromatographymass spectrometry (GC-MS), immunoassays, and HPLC with single MS detection (Cadet et al. , 2012a. Considerable progress has also been made in the elucidation of oxidative degradation pathways of isolated DNA and related model compounds (for recent comprehensive reviews, see Gimisis and Cismaş 2006;Neeley and Essigmann 2006;Pratviel and Meunier 2006;von Sonntag 2006;Cadet et al. 2008Cadet et al. , 2010Cadet et al. , 2012bDedon 2008;Burrows 2009;Wagner and Cadet 2010). In addition, there is much complementary information on solar-radiation-induced formation of bipyrimidine photoproducts in the DNA of fibroblasts, keratinocytes, and human skin. In particular, the distribution of UVA and UVB photoproducts has been determined, allowing accurate determination of their rates of repair (Cadet et al.

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Section: Uva-mediated Formation Of Cyclobutane Pyrimidine Dimersmentioning

confidence: 81%

Section: Uva-mediated Formation Of Cyclobutane Pyrimidine Dimersmentioning

confidence: 91%

DNA Base Damage by Reactive Oxygen Species, Oxidizing Agents, and UV Radiation

Cadet

Wagner

2013

Cold Spring Harbor Perspectives in Biology

720

510

View full text Add to dashboard Cite

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“…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. However, these observations have been poorly considered until recently.…”

Section: Uva-induced Cpdsmentioning

confidence: 99%

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions^†

Cadet¹,

Mouret²,

Ravanat³

et al. 2012

Photochem & Photobiology

271

251

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The survey focuses on recent aspects of photochemical reactions to cellular DNA that are implicated through the predominant formation of mostly bipyrimidine photoproducts in deleterious effects of human exposure to sunlight. Recent developments in analytical methods have allowed accurate and quantitative measurements of the main DNA photoproducts in cells and human skin. Highly mutagenic CC and CT bipyrimidine photoproducts, including cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) are generated in low yields with respect to TT and TC photoproducts. Another striking finding deals with the formation of Dewar valence isomers, the third class of bipyrimidine photoproducts that is accounted for by UVA-mediated isomerization of initially UVB generated 6-4PPs. Cyclobutadithymine (T< >T) has been unambiguously shown to be involved in the genotoxicity of UVA radiation. Thus, T< >T is formed in UVA-irradiated cellular DNA according to a direct excitation mechanism with a higher efficiency than oxidatively generated DNA damage that arises mostly through the Type II photosensitization mechanism. C<>C and C< >T are repaired at rates intermediate between those of T< >T and 6-4TT. Evidence has been also provided for the occurrence of photosensitized reactions mediated by exogenous agents that act either in an independent way or through photodynamic effects.

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“…[10] Given this fact, it seems at first not likely that UVA-1 might be capable of a significant IL-6 induction in vivo. However, recent work by Tewari et al [11] in vivo has demonstrated the capability of UVA-1 to also induce CPD in significant amounts. Thus, the DNA damage-related mechanism of IL-6 release was shown to exist also for the UVA-1 spectrum in vivo and this fits with our data.…”

Section: Discussionmentioning

confidence: 99%

UVA‐1 exposure in vivo leads to an IL‐6 surge within the skin

Schneider

Raizner²,

Wlaschek³

et al. 2017

Experimental Dermatology

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UVA-1 is a known promotor of skin ageing. Cytokines like IL-1α, Il-1β or TNF-α, VEGF and IL-6 orchestrate UV effects, and IL-6 is furthermore an effector of UVA-induced photoageing. We investigated how fractionated UVA-1 doses influence the cytokine milieu and especially the IL-6 levels in the skin in vivo. In a study with 35 participants, we exposed previously unirradiated human skin to three UVA-1 irradiation regimes. Cytokine levels in interstitial skin fluid were measured up to 48 hours postexposure and compared to unirradiated control skin fluid. Our results show that IL-6 levels increased significantly after UVA-1 exposure at selected time points. The other candidates IL-1α, Il-1β or TNF-α and VEGF show no significant response after UVA-1 exposure in vivo. UVA-1 thus raises selectively IL-6 levels in vivo, a fact that underlines its role in photoageing and has potential implications for its modulatory effect on photoageing pathology.

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UVA1 Induces Cyclobutane Pyrimidine Dimers but Not 6-4 Photoproducts in Human Skin In Vivo

Cited by 125 publications

References 46 publications

DNA Base Damage by Reactive Oxygen Species, Oxidizing Agents, and UV Radiation

DNA Base Damage by Reactive Oxygen Species, Oxidizing Agents, and UV Radiation

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions^†

UVA‐1 exposure in vivo leads to an IL‐6 surge within the skin

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UVA1 Induces Cyclobutane Pyrimidine Dimers but Not 6-4 Photoproducts in Human Skin In Vivo

Cited by 125 publications

References 46 publications

DNA Base Damage by Reactive Oxygen Species, Oxidizing Agents, and UV Radiation

DNA Base Damage by Reactive Oxygen Species, Oxidizing Agents, and UV Radiation

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions†

UVA‐1 exposure in vivo leads to an IL‐6 surge within the skin

Contact Info

Product

Resources

About

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions^†