Skin DNA photodamage and its biological consequences

Marrot, Laurent; Meunier, Jean‐Roch

doi:10.1016/j.jaad.2007.12.007

Cited by 294 publications

(248 citation statements)

References 70 publications

(61 reference statements)

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“…Stork et al 15 described that the elevation of intracellular zinc levels after UVB irradiation is proportional to the fraction of dying or dead cells, and they concluded that UVB-induced zinc release may be an important step in UVB-induced cell death pathways. The consequences of UVB-induced direct (primarily CPDs) and indirect (free radical generation) DNA damage are cell cycle arrest, DNA repair, and the induction of cell death pathways causing sunburn, inflammation, immunosuppression, and melanogenesis in the skin 47 . We measured both the CPD level and superoxide generation (Figure 3c and 3d).…”

Section: Discussionmentioning

confidence: 99%

Effects of non-toxic zinc exposure on human epidermal keratinocytes

et al. 2015

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Zinc is an essential microelement; its importance to skin is shown by severe skin symptoms in hereditary or acquired zinc deficiency, by the improvement of several skin conditions using systemic or topical zinc preparations and by the induced intracellular zinc release upon UVB exposure, which is the main harmful environmental factor to skin. Understanding the molecular background of the role of zinc in skin may help to gain insight into the pathology of skin disorders and to provide evidence for the therapeutic usefulness of zinc supplementation.Herein, we studied the effect of zinc chloride (ZnCl 2 ) exposure on the function of HaCaT keratinocytes, and we found that a non-toxic elevation in the concentration of extracellular zinc (100 µM) facilitated cell proliferation and induced significant alterations in the mRNA expression of NOTCH1, IL8, and cyclooxygenase-2. In addition, we detected increased heme oxygenase-1 (HMOX1) expression and non-toxic generation of superoxide in the first 4 h.Regarding the effect on UVB-induced toxicity, although the level of cyclobutane pyrimidine dimers in keratinocytes pre-treated with zinc for 24 h was reduced 3 h after UVB irradiation, we found significantly enhanced superoxide generation 10 h after UVB exposure in the zinc pre-exposed cells. The overall survival was unaffected; however, there was a decrease in the percentage of early apoptotic cells and an increase in the percentage of late apoptotic plus necrotic cells.Our results suggest that exposure of human keratinocytes to non-toxic concentrations of ZnCl 2 impacts gene expression, cell proliferation and the response to environmental stress in skin. It would be important to further examine the role of zinc in skin and to further clarify if this issue can affect our thinking about the pathogenesis of skin diseases.

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Section: Discussionmentioning

confidence: 99%

Effects of non-toxic zinc exposure on human epidermal keratinocytes

et al. 2015

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“…However, it must be noted that CPDs are also produced routinely in human skin by sunlight as well. The UV component of sunlight is mainly responsible for this [15,16]. An individual is therefore already at a certain risk for skin carcinogenesis, especially squamous cell carcinoma (SCC) due to chronic exposure to sunlight [17,18].…”

Section: Biophotonicsmentioning

confidence: 99%

“…Sunlight UV can therefore serve as the reference point for NLO imaging with regard to cancer risk studies in skin, since sunlight UV is already known to cause SCC in the skin via CPDs [16,18,31], Since NLO imaging primarily deals with wavelengths in the range from 700-800 nm, it is essential to know how CPDs produced from MPE processes with pulsed NIR wavelength light compare with UV action spectra for CPDs. It was previously known that the UVC (230-280 nm) and UVB components (280-320 nm) of sunlight were mainly responsible for CPD formation and eventual carcinogenesis [15,16]. So a 3-photon process from the laser would result in absorption between 233-267 nm, lying in UVC region, resulting in CPD production.…”

Section: Role Of Sunlight Uv and Multi-photon Processes In The Risk Mmentioning

confidence: 99%

“…Since these lesions are also formed in the UVA range, mainly at 360-400 nm [15], more insight is also needed for the carcinogenesis risk from these lesions as well, especially in case of 2-photon processes from imaging wavelengths between 720-800 nm. In addition, 3-photon processes for wavelengths above 800 nm at high peak intensity can produce CPDs as well, as these MPE processes would be equivalent for UVB irradiation lying between 280-320 nm.…”

Section: Limitations Of the Modelmentioning

confidence: 99%

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Estimating the risk of squamous cell cancer induction in skin following nonlinear optical imaging

Thomas

Nadiarnykh

Voskuilen

et al. 2013

Journal of Biophotonics

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High power femto‐second (fs) laser pulses used for in‐vivo nonlinear optical (NLO) imaging can form cyclobutane pyrimidine dimers (CPD) in DNA, which may lead to carcinogenesis via subsequent mutations. Since UV radiation from routine sun exposure is the primary source of CPD lesions, we evaluated the risk of CPD‐related squamous cell carcinoma (SCC) in human skin due to NLO imaging relative to that from sun exposure. We developed a unique cancer risk model expanding previously published estimation of risk from exposure to continuous wave (CW) laser. This new model showed that the increase in CPD‐related SCC in skin from NLO imaging is negligible above that due to regular sun exposure. (© 2014 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)

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“…This damage leads to the development of skin cancer. 12 In particular, most epidemiological studies found that sun exposure in childhood and intense intermittent sun exposure are likely to be the major environmental risk factors for the development of melanoma. Irregular and intense exposure to sunlight significantly increases the risk.…”

mentioning

confidence: 99%