Environmental Factors in Nonmelanoma and Melanoma Skin Cancer

Woodhead, Avril D.; Setlow, R. B.; Tanaka, Michiko

doi:10.2188/jea.9.6sup_102

Cited by 83 publications

(63 citation statements)

References 87 publications

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“…Besides its well-known advantages and its indispensable effects on human life, UV radiation, in particular the middle wavelength (UVB, range 290 -320 nm), can be a hazard to human health by inducing cancer, premature skin aging, immunosuppression, inflammation, and cell death (1)(2)(3)(4)(5). Accordingly, the incidence of UV-induced skin cancer is rapidly rising, accounting for Ͼ40% of all human cancers in the United States (6). UV-induced DNA damage is one of the major molecular events when a cell is hit by UV radiation.…”

Section: Il-18mentioning

confidence: 99%

IL-18 Reduces Ultraviolet Radiation-Induced DNA Damage and Thereby Affects Photoimmunosuppression

Schwarz

Maeda

Ständer

et al. 2006

The Journal of Immunology

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UV-induced DNA damage has been recognized as the major molecular trigger for photoimmunosuppression. IL-12 prevents UV-induced immunosuppression via its recently discovered capacity to reduce DNA damage presumably via induction of DNA repair. Because IL-18 shares some biological activities with IL-12 we studied the effect of IL-18 on UV-induced DNA damage and immunosuppression. IL-18 reduced UV-induced apoptosis of keratinocytes and supported long-term cell survival on UV exposure. Injection of IL-18 into mice that were exposed to UV radiation significantly lowered the number of apoptotic keratinocytes. Accordingly, radiation immunohistochemistry revealed reduced amounts of DNA damage in epidermal cells upon injection of IL-18. These effects were not observed in DNA repair-deficient (XpaKO) mice, indicating that IL-18 like IL-12 reduces DNA damage via DNA repair. UV-mediated suppression of the induction of contact hypersensitivity, which is known to be primarily triggered by DNA damage, was prevented upon injection of IL-18 before UV exposure in wild-type but not in XpaKO mice. In contrast to IL-12, IL-18 was not able either in wild-type or in XpaKO mice to break UV-induced immunotolerance that is mediated via regulatory T cells rather than in a DNA damage-dependent fashion. This result indicates that IL-12 is still unique in its capacity to restore immune responses because of its effect on regulatory T cells. Together, these data identify IL-18 as a further cytokine that exhibits the capacity to affect DNA repair. Though being primarily a proinflammatory cytokine through this capacity, IL-18 can also foster an immune response that is suppressed by UV radiation.

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Section: Il-18mentioning

confidence: 99%

IL-18 Reduces Ultraviolet Radiation-Induced DNA Damage and Thereby Affects Photoimmunosuppression

Schwarz

Maeda

Ständer

et al. 2006

The Journal of Immunology

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“…Ultraviolet (UV) radiation induces basal and squamous cell carcinoma and cutaneous malignant melanoma in humans [1][2][3] and is therefore a major environmental concern. UV radiations exert their toxic effects by causing DNA damage, which depends mainly on the wavelength.…”

Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Masuma

Kashima

Kurasaki

et al. 2013

Journal of Photochemistry and Photobiology B: Biology

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Ultraviolet (UV) radiations present in sunlight are a major etiologic factor for many skin diseases and induce DNA damage through formation of cyclobutane pyrimidine dimer (CPD). This study was conducted to determine the toxicological effects of different wavelengths (250, 270, 290, and 310 nm) and doses of UV radiation on cell viability, DNA structure, and DNA damage repair mechanisms in a PC12 cell system. For this, we evaluated cell viability and CPD formation. Cell survival rate was markedly decreased 24 h after UV irradiation in a dose-dependent manner at all wavelengths (except at 310 nm). Cell viability increased with increasing wavelength in the following order: 250 < 270 < 290 < 310 nm. UV radiation at 250 nm showed the highest cell killing ability, with a median lethal dose (LD50) of 120 mJ/cm2. The LD50 gradually increased with increase in wavelength. Among the 4 wavelengths tested, the highest LD50 (6000 mJ/cm2) was obtained for 310 nm. CPD formation decreased substantially with increasing wavelength. Among the 4 wavelengths, the proportion of CPD formation was highest at 250 nm and lowest at 310 nm. On the basis of LD50 values for each wavelength, PC12 cells irradiated with UV radiation of 290 nm showed maximum DNA repair ability, whereas those irradiated with the 310-nm radiation did not show any repair ability. Toxicity of UV radiation varied with wavelengths and exposure doses

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“…The induction of cII mutant frequency was effectively reduced consequent to a cotreatment with vitamin C. Our findings support the notion that UVA-induced photosensitization reactions are responsible for oxidative DNA damage leading to mutagenesis. ultraviolet A radiation ͉ photosensitizer ͉ antioxidant ͉ skin cancer A large body of evidence exists regarding the association between solar UV irradiation and human skin carcinogenesis (1,2). Sunlight UV wavelengths that reach the surface of the earth are UVA (Ͼ320-400 nm) and UVB (280-320 nm), with shorter wavelengths (UVC) being completely absorbed by stratospheric oxygen (O 2 ) (1, 3).…”

mentioning

confidence: 99%

Riboflavin activated by ultraviolet A1 irradiation induces oxidative DNA damage-mediated mutations inhibited by vitamin C

Besaratinia

Kim

Bates

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

100

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An increasingly popular theory ascribes UVA (>320 -400 nm) carcinogenicity to the ability of this wavelength to trigger intracellular photosensitization reactions, thereby giving rise to promutagenic oxidative DNA damage. We have tested this theory both at the genomic and nucleotide resolution level in mouse embryonic fibroblasts carrying the lambda phage cII transgene. We have also tested the hypothesis that inclusion of a cellular photosensitizer (riboflavin) can intensify UVA-induced DNA damage and mutagenesis, whereas addition of an antioxidant (vitamin C) can counteract the induced effects. Cleavage assays with formamidopyrimidine DNA glycosylase (Fpg) coupled to alkaline gel electrophoresis and ligation-mediated PCR (LM-PCR) showed that riboflavin treatment (1 M) combined with UVA1 (340 -400 nm) irradiation (7.68 J/cm 2 ) or higher dose UVA1 irradiation alone induced Fpg-sensitive sites (indicative of oxidized and/or ring-opened purines) in the overall genome and in the cII transgene, respectively. Also, the combined treatment with riboflavin and UVA1 irradiation gave rise to single-strand DNA breaks in the genome and in the cII transgene determined by terminal transferasedependent PCR (TD-PCR). A cotreatment with vitamin C (1 mM) efficiently inhibited the formation of the induced lesions. Mutagenicity analysis showed that riboflavin treatment combined with UVA1 irradiation or high-dose UVA1 irradiation alone significantly increased the relative frequency of cII mutants, both mutation spectra exhibiting significant increases in the relative frequency of G:C 3 T:A transversions, the signature mutations of oxidative DNA damage. The induction of cII mutant frequency was effectively reduced consequent to a cotreatment with vitamin C. Our findings support the notion that UVA-induced photosensitization reactions are responsible for oxidative DNA damage leading to mutagenesis. ultraviolet A radiation ͉ photosensitizer ͉ antioxidant ͉ skin cancer A large body of evidence exists regarding the association between solar UV irradiation and human skin carcinogenesis (1, 2). Sunlight UV wavelengths that reach the surface of the earth are UVA (Ͼ320-400 nm) and UVB (280-320 nm), with shorter wavelengths (UVC) being completely absorbed by stratospheric oxygen (O 2 ) (1, 3). The biologically relevant UVA and UVB have been extensively studied as the etiologic factors for skin cancer (4). The mechanistic involvement of UVB in carcinogenesis rests upon the ability of this wavelength to induce promutagenic cis-syn cyclobutane pyrimidine dimers (CPDs), pyrimidine (6-4) pyrimidone photoproducts ((6-4)PPs), and Dewar valence photoisomers (4). However, the underlying mechanism of action for UVA carcinogenicity is not fully delineated (4). Despite the weak absorbance of UVA by DNA (3), a genotoxic mode of action for UVA has been demonstrated (1). Yet, the exact process through which UVA exerts genotoxicity remains elusive (4).A widely recognized theory ascribes UVA genotoxicity to its ability to trigger intracellular photosensitizat...

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Environmental Factors in Nonmelanoma and Melanoma Skin Cancer

Cited by 83 publications

References 87 publications

IL-18 Reduces Ultraviolet Radiation-Induced DNA Damage and Thereby Affects Photoimmunosuppression

IL-18 Reduces Ultraviolet Radiation-Induced DNA Damage and Thereby Affects Photoimmunosuppression

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Riboflavin activated by ultraviolet A1 irradiation induces oxidative DNA damage-mediated mutations inhibited by vitamin C

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