Erythema, skin cancer risk, and sunscreens

Naylor, M. F.

doi:10.1001/archderm.133.3.373

Cited by 18 publications

(19 citation statements)

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“…18 The delayed UV-induced erythema (ie, sunburn) may cause the fading of the border and of the pigment network structures because of an increase of blood flow and induction of an inflammatory infiltrate triggered mainly by prostaglandins and by the damage to DNA. 8 The dermoscopic changes of melanocytic nevi observed in the present study are also somehow in accordance with histopathologic findings of nevi excised in summer months, which showed significantly more mitoses and inflammatory infiltrate compared with nevi excised in winter months. 19,20 Three studies have already focused on the impact of UV irradiation on the dermoscopic appearance of melanocytic nevi.…”

Section: Commentsupporting

confidence: 90%

“…1998;134:845-850 U LTRAVIOLET radiation is considered one of the most important agents of skin cancer, although its exact role in the development of benign and malignant melanocytic skin tumors remains unclear. [1][2][3][4][5][6][7][8] Results of several epidemiological studies indicate that intermittent exposure to UV radiation is especially linked to the development of a higher number of nevi. 9,10 Moreover, sunburns during childhood seem to be an independent risk factor for the development of malignant melanoma.…”

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confidence: 99%

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Ultraviolet Radiation of Melanocytic Nevi

Hofmann-Wellenhof

Soyer²,

Wolf³

et al. 1998

Arch Dermatol

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Section: Commentsupporting

confidence: 90%

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confidence: 99%

Ultraviolet Radiation of Melanocytic Nevi

Hofmann-Wellenhof

Soyer²,

Wolf³

et al. 1998

Arch Dermatol

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“…In addition, exposure to solar UV radiation is known to induce erythema, edema, sunburn cell formation, a hyperplastic response, immune suppression and photoaging (2,(5)(6)(7). It has long been regarded that photochemical damage induced by UV in chromosomal DNA of skin cells, predominantly in the form of cyclobutane pyrimidine dimers (CPD) † plays an essential role in skin cancer induction.…”

Section: Introductionmentioning

confidence: 99%

Kinetics of UV Light-induced Cyclobutane Pyrimidine Dimers in Human Skin In Vivo: An Immunohistochemical Analysis of both Epidermis and Dermis

Katiyar¹,

Matsui²,

Mukhtar³

2007

Photochemistry and Photobiology

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It is well known that UV exposure of human skin induces DNA damage, and the cumulative effect of such repeated damage is an important contributor to the development of skin cancer. Here, we demonstrate UV dose‐ and time‐dependent induction of DNA damage in the form of cyclobutane pyrimidine dimers (CPD) in skin cells following a single exposure of human skin to UV radiation. CPD+ cells were identified by an immunohistochemical technique using monoclonal antibodies to thymine dimers. The percentage of CPD+ cells was UV dose–dependent, even a suberythemal (0.5 minimal erythemal dose [MED]) dose resulted in detectable level of cells that contained pyrimidine dimers. Forty‐eight hours after irradiation the percent of total epidermal cells positive for CPD ranged from 19 ± 8, 36 ± 10, 57 ± 12 and 80 ± 10, and total percent dermal cells positive for CPD ranged from 1 ± 1, 7 ± 3, 16 ± 3 and 20 ± 5, respectively, following 0.5, 1.0, 2.0 and 4.0 MED. CPD were also observed in deeper reticular dermis, which suggest the penetrating ability of UV radiation into the skin. The change in CPD+ cells from 0.5 to 240 h post‐UV exposure in both epidermal and dermal compartments of the skin was also quantitated. CPD+ cells were observed in skin biopsies at early time points after UV exposure which remained elevated for 48 h, then declined significantly by 3 days post‐UV. A close examination of the skin at and after 3 days following UV exposure indicates the significant removal of DNA damaged cells from the epidermis. Ten days after UV exposure the levels of CPD+ cells in both epidermis and dermis were not significantly different from that in unirradiated skin.

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“…The primary defect causing the inflammation appears to be epidermal DNA damage (6). Since the protection from, or repair of, DNA lesions is associated with protection from photocarcinogenesis in chronically exposed skin, the acute inflammatory sunburn reaction may be considered as a biomarker for photocarcinogenesis risk (7).…”

Section: Introductionmentioning

confidence: 99%

Isoflavonoid Compounds from Red Clover (Trifolium pratense) Protect from Inflammation and Immune Suppression Induced by UV Radiation¶

Widyarini

Spinks²,

Husband³

et al. 2001

Photochem Photobiol

124

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Isoflavones derived from many edible plants have been reported to possess significant antioxidant, estrogenic and tyrosine kinase inhibitory activity. Genistein has been found previously to provide protection from oxidative damage induced by UV radiation both in vitro and following dietary administration. We have therefore examined the potential of a number of isoflavones from red clover (Trifolium pratense) and some metabolically related compounds to offer protection from UV irradiation in hairless mice by topical application after UV exposure. We show that whereas the primary isoflavones, daidzein, biochanin A and formononetin, were inactive, 20 microM lotions of genistein and the metabolites equol, isoequol and the related derivative dehydroequol had powerful potential to reduce the inflammatory edema reaction and the suppression of contact hypersensitivity induced by moderate doses of solar-simulated UV radiation. For equol the protection was concentration dependent and 5 microM equol markedly reduced the UV-induced inflammation but abrogated the UV-induced immunosuppression. Equol protected similarly from immunosuppression induced by the putative epidermal mediator, cis-urocanic acid (UCA), indicating a potential mechanism of action involving inactivation of this UV-photoproduct. Since immunosuppression induced by both UV radiation and by cis-UCA appears to be an oxidant-dependent response our observations support the actions of these topically applied isoflavones and their metabolites as antioxidants. They also indicate that lotions containing equol, unlike topical UV sunscreens, more readily protect the immune system from photosuppression than from the inflammation of the sunburn reaction, even when applied after exposure, and thus such compounds may have a future role as sun-protective cosmetic ingredients.

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Erythema, skin cancer risk, and sunscreens

Cited by 18 publications

References 0 publications

Ultraviolet Radiation of Melanocytic Nevi

Ultraviolet Radiation of Melanocytic Nevi

Kinetics of UV Light-induced Cyclobutane Pyrimidine Dimers in Human Skin In Vivo: An Immunohistochemical Analysis of both Epidermis and Dermis

Isoflavonoid Compounds from Red Clover (Trifolium pratense) Protect from Inflammation and Immune Suppression Induced by UV Radiation¶

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