Photoprotection by 1α,25-dihydroxyvitamin D and analogs: Further studies on mechanisms and implications for UV-damage

Mason, Rebecca S.; Sequeira, Vanessa B.; Dixon, Katie M.; Gordon-Thomson, Clare; Pobre, Kristine Faye R.; Dilley, A.; Mizwicki, Mathew T.; Norman, Anthony W.; Feldman, David; Halliday, Gary M.; Reeve, Vivienne E.

doi:10.1016/j.jsbmb.2010.03.082

Cited by 70 publications

(64 citation statements)

References 38 publications

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“…Our previous studies, and those of others, provide compelling evidence for novel photoprotective effects of vitamin D compounds in human skin cells and in hairless mice (17)(18)(19)(20)(21)(22)(23)(24). These studies were limited to investigation of the effects of an application of these compounds in acute UVRinduced skin damage, including cell loss and formation of DNA lesions in the form of CPDs and preliminary studies on photo immunosuppression.…”

Section: Introductionmentioning

confidence: 97%

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

Dixon

Norman

Sequeira

et al. 2011

Cancer Prevention Research

107

153

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Exposure to ultraviolet radiation (UVR) can lead to a range of deleterious responses in the skin. An important form of damage is the DNA photolesion cyclobutane pyrimidine dimer (CPD). CPDs can be highly mutagenic if not repaired prior to cell division and can lead to UV-induced immunosuppression, making them potentially carcinogenic. UVR exposure also produces vitamin D, a prehormone. Different shapes of the steroid hormone 1a,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] can produce biological responses through binding either to its cognate nuclear receptor (VDR) to regulate gene transcription or to the VDR associated with plasma membrane caveolae to produce, via signal transduction, nongenomic physiologic responses. Here, we show that both 1,25(OH) 2 D 3 and 1a,25(OH) 2 -lumisterol (JN), a conformationally restricted analogue that can generate only nongenomic responses, are effective inhibitors of UV damage in an immunocompetent mouse (Skh:hr1) model susceptible to UV-induced tumors. Both 1,25(OH) 2 D 3 and JN significantly reduced UVR-induced CPD, apoptotic sunburn cells, and immunosuppression. Furthermore, these compounds inhibited skin tumor development, both papillomas and squamous cell carcinomas, in these mice. The observed reduction of these UV-induced effects by 1,25 (OH) 2 D 3 and JN suggests a role for these compounds in prevention against skin carcinogenesis. To the best of our knowledge, this is the first comprehensive report of an in vivo long-term biological response generated by chronic dosing with a nongenomic-selective vitamin D steroid.

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Section: Introductionmentioning

confidence: 97%

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

Dixon

Norman

Sequeira

et al. 2011

Cancer Prevention Research

107

153

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“…In the skin, mechanisms of endogenous photoprotection following sun exposure include, among others, increased pigmentation via melanocytes and increased cornification of keratinocytes. It has been previously reported that calcitriol could enhance these processes [35] . Vitamin D can be converted to 1,25(OH) 2 D 3 due to the presence of vitamin D-25 hydroxylase and 25(OH)D-1α-hydroxylase in keratinocytes [7] , though the process takes several hours.…”

Section: Discussionmentioning

confidence: 96%

“…Vitamin D can be converted to 1,25(OH) 2 D 3 due to the presence of vitamin D-25 hydroxylase and 25(OH)D-1α-hydroxylase in keratinocytes [7] , though the process takes several hours. This suggests that formation of 1,25(OH) 2 D 3 in the skin seems to protect against the next rather than the initial UV irradiation [12] , implying that exogenous analogues of calcitriol could represent an added value in sunscreens [35] .…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Supplementation Does Not Improve the Severity or the Resolution of Ultraviolet B-Induced Acute Erythema

Libon¹,

Seidel²,

Cavalier

et al. 2015

Dermatology

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Background: Whether vitamin D supplementation alleviates the severity of ultraviolet B (UVB)-induced erythema and/or facilitates its resolution remains undetermined. Objective: To study the effect of oral vitamin D on UVB-induced erythema and its resolution in fair-skinned subjects. Methods: UVB-induced erythema was quantified using a Chroma Meter® in 50 volunteers 48 h before and 10 days after the random administration of 200,000 IU vitamin D (n = 40) or placebo (n = 10). Resolution of erythema in both groups was assessed by chromametry 24, 48, and 72 h after vitamin D administration. Results: No statistical difference between erythema values before and after administration in the vitamin D-supplemented group (p = 0.44) or the placebo group (p = 0.34) was noted. No statistical difference was evident between both groups with respect to resolution of erythema (p = 0.30). Conclusion: Oral vitamin D supplementation neither improves protection against UVB-induced erythema nor facilitates its resolution.

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“…26,27 Estes estudos levantam também a possibilidade de, no que diz respeito à prevenção do melanoma, a ação local da vitamina D ser pelo menos tão significativa que a sua ação sistémica. Consideramos ser importante a investigação neste sentido.…”

Section: Melanoma E Exposição Solarunclassified

Vitamina D e Melanoma

Silva

Teixeira

Correia

2017

SPDV

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RESUMO -A vitamina D participa na homeostasia do cálcio e mineralização óssea. Recentemente, a vitamina D foi implicada na patogénese do cancro e, mais especificamente, do melanoma. A deficiência sérica de 25(OH)D3, o precursor da forma ativa da vitamina D, tem sido associado ao aumento da incidência e a pior prognóstico do melanoma. Em modelos in vitro de vários tumores, a suplementação de vitamina D tem ação anti-inflamatória e promove a apoptose, induz a diferenciação, inibe a proliferação e sensibiliza as células tumorais para terapias anti-tumorais. Também a modulação da expressão dos recetores da vitamina D (VDR) parece estar implicada no efeito anti-tumoral da vitamina D. A relação entre a vitamina D e o melanoma torna-se mais controversa quando a obtenção de vitamina D através da exposição à radiação ultra-violeta pode estar associado ao aumento do risco de melanoma. Neste artigo é efetuada revisão da literatura e dadas sugestões de atuação no que se refere à exposição solar, níveis séricos de vitamina D e redução da incidência e gravidade do melanoma. PALAVRAS-CHAVE - INTRODUÇÃOAo longo dos últimos anos, nenhuma vitamina foi tão exaustivamente estudada na sua possível relação com a carcinogénese e no prognóstico de doentes com neoplasia quanto a vitamina D.1 Nos últimos 20 anos têm sido verificados progressos consideráveis no sentido de esclarecer e aprofundar o seu papel neste grupo de patologias através de estudos epidemiológicos e experimentais.2 Existiu também um avanço muito significativo durante o último século na compreensão da sua formação e ativação. Com este artigo procuramos ajudar a esclarecer, de forma simples e atual, algumas questões relativas à vitamina D e à sua relação com o melanoma, abordando a dicotomia que parece existir entre o facto da síntese de vitamina D depender da exposição solar e ter um efeito protetor quanto à carcinogénese e, por outro lado, a exposição solar ser um fator de risco para o desenvolvimento do melanoma. VITAMINA D: COMO É SINTETIZADA E QUAL O SEU PAPEL NO ORGANISMO?A vitamina D é uma pro-hormona lipossolúvel produzida pela pele a partir da exposição à radiação ultravioleta B

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Photoprotection by 1α,25-dihydroxyvitamin D and analogs: Further studies on mechanisms and implications for UV-damage

Cited by 70 publications

References 38 publications

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

Vitamin D Supplementation Does Not Improve the Severity or the Resolution of Ultraviolet B-Induced Acute Erythema

Vitamina D e Melanoma

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