Extensive proof that Vitamin D protects DNA in skin from UV damage
Observation: People get a sunburn when getting lots of sun after months of little sun.
Question: Would they not get a sunburn if they first stocked up on vitamin D?
Table of contents
- Sunlight and vitamin D affect DNA damage, cell division and cell death in human lymphocytes: a cross-sectional study in South Australia.
- 1?,25 Dihydroxyvitamin D(3) enhances cellular defences against UV-induced oxidative and other forms of DNA damage in skin.
- Perspective Protective actions of vitamin D in UVB induced skin cancer
- Active vitamin D protects skin against sunlight damage – Nov 2012
- Vitamin D and Death by Sunshine
- Biologically efficient solar radiation: Vitamin D production and induction of cutaneous malignant melanoma
- See also VitaminDWiki
Sunlight and vitamin D affect DNA damage, cell division and cell death in human lymphocytes: a cross-sectional study in South Australia.
Mutagenesis. 2012 Sep;27(5):609-14. doi: 10.1093/mutage/ges026. Epub 2012 Apr 29.
Nair-Shalliker V, Fenech M, Forder PM, Clements MS, Armstrong BK.
Sydney School of Public Health, The University of Sydney, Sydney, New South Wales 2006, Australia. visalinin at nswcc.org.au
The ultraviolet (UV)-B spectrum in solar UV radiation is essential for stimulating the epidermal production of vitamin D but also damages DNA and causes cancer in exposed cells. We examined the role of solar UV in inducing DNA damage in blood lymphocytes and the possible modulation of this damage by serum 25-hydroxy vitamin D (25(OH)D) in 207 male and female participants from South Australia. Personal solar UV exposure was estimated from hours of outdoor exposure recalled at the time of blood collection for analysis of DNA damage in lymphocytes, using the cytokinesis-block micronucleus cytome (CBMN-cyt) assay and of serum 25(OH)D.
We examined the association between solar UV exposure, serum 25(OH)D and DNA damage using multiple linear regression, with age, sex, body mass index and alcohol consumption as covariates.
The frequency of cells with micronuclei (a biomarker of chromosome breakage or loss) increased with increasing sun exposure [% increase = 5.24; 95% confidence interval (CI): 0.35 to 10.37 P-value = 0.04]
but cells with nucleoplasmic bridges (a biomarker of misrepair of DNA strand breaks or telomere end fusions) decreased (% increase = -8.38; 95% CI: -14.32 to -2.03 P-value = 0.01).
There was also a fall in the nuclear division index (NDI) (% increase = -1.01; 95% CI: -2.00 to 0.00 P-value = 0.05), suggesting diminished mitogenic response and, possibly, immune suppression.
There was no overall relationship between 25(OH)D and DNA damage.
There were, however, weak modulating effects of 25(OH)D on the associations of solar UV exposure with micronucleus formation and with NDI (P-interaction = 0.03 and 0.05, respectively), where the increase in micronuclei and fall in NDI with increasing solar UV were greater at serum 25(OH)D levels <50 nmol/l.
Thus, the influence of solar UV exposure in causing DNA damage or immune suppression in internal tissues may be stronger when vitamin D levels are low.
1?,25 Dihydroxyvitamin D(3) enhances cellular defences against UV-induced oxidative and other forms of DNA damage in skin.
Photochem Photobiol Sci. 2012 Oct 15.
Gordon-Thomson C, Gupta R, Tongkao-On W, Ryan A, Halliday GM, Mason RS.
Department of Physiology, The Bosch Institute, The University of Sydney, NSW 2006, Australia. rebeccam at physiol.usyd.edu.au.
DNA damage induced by ultraviolet radiation is the key initiator for skin carcinogenesis since mutations may arise from the photoproducts and it also contributes to photoimmune suppression. The active vitamin D hormone, 1?,25 dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) reduces thymine dimers, the major photoproduct found in human skin after UV exposure, and suppresses the accumulation of nitric oxide derivatives that lead to more toxic reactive nitrogen species (RNS). We examined whether other forms of DNA damage are reduced by 1,25(OH)(2)D(3), and hypothesized that photoprotection by 1,25(OH)(2)D(3) is, in part, due to the suppression of various forms of promutagenic DNA damage, including thymine dimers, through a reduction of genotoxic RNS. Different forms of UV-induced DNA damage were investigated in irradiated skin cells treated with or without 1,25(OH)(2)D(3), or inhibitors of metabolism and inducible nitric oxide synthase. Keratinocytes were also treated with nitric oxide donors in the absence of UV light. DNA damage was assessed by comet assay incorporating site specific DNA repair endonucleases, and by immunohistochemistry using antibodies to thymine dimers or 8 - oxo-7,8-dihydro-2'-deoxyguanosine, and quantified by image analysis. Strand breaks in T4 endonuclease V, endonuclease IV and human 8 - oxoguanine DNA glycosylase digests increased more than 2-fold in UV irradiated human keratinocytes, and were reduced by 1,25(OH)(2)D(3) treatment after UV exposure, and m azide and an inhibitor of inducible nitric oxide synthase. Conversely, nitric oxide donors induced all three types of DNA damage in the absence of UV.
We present data to show that 1,25(OH)(2)D(3) protects skin cells from at least three forms of UV-induced DNA damage, and provide further evidence to support the proposal that a reduction in RNS by 1,25(OH)(2)D(3) is a likely mechanism for its photoprotective effect against oxidative and nitrative DNA damage, as well as cyclobutane pyrimidine dimers.
Daniel D. Bikle
Photochem. Photobiol. Sci., 2012, Advance Article
Received 11 Jul 2012, Accepted 27 Aug 2012, First published on the web 29 Aug 2012
Non-melanoma skin cancers (NMSC) are the most common type of cancer, occurring at a rate of over 1 million per year in the United States. Although their metastatic potential is generally low, they can and do metastasize, especially in the immune compromised host, and their surgical treatment is often quite disfiguring. Ultraviolet radiation (UVR) as occurs with sunlight exposure is generally regarded as causal for these malignancies, but UVR is also required for vitamin D synthesis in the skin. Based on our own data and that reported in the literature, we hypothesize that the vitamin D produced in the skin serves to suppress UVR epidermal tumor formation. In this review we will first discuss the evidence supporting the conclusion that the vitamin D receptor (VDR), with or without its ligand 1,25-dihydroxyvitamin D, limits the propensity for cancer formation following UVR.
We will then explore three potential mechanisms for this protection:
- inhibition of proliferation and stimulation of differentiation,
- immune regulation, and
- stimulation of DNA damage repair (DDR).
1α,25-Dihydroxyvitamin D(3) reduces several types of UV-induced DNA damage and contributes to photoprotection.
J Steroid Biochem Mol Biol. 2012 Nov 16. pii: S0960-0760(12)00236-1.
Song EJ, Gordon-Thomson C, Cole L, Stern H, Halliday GM, Damian DL, Reeve VE, Mason RS.
Department of Physiology and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
Vitamin D production requires UVB. In turn, we have shown that vitamin D compounds reduce UV- induced damage, including inflammation, sunburn, thymine dimers, the most frequent type of cyclobutane pyrimidine dimer, immunosuppression, and photocarcinogenesis. Our previous studies have shown most of the photoprotective effects by 1α,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) occurred through the nongenomic pathway because similar protection was seen with an analog, 1α,25-dihydroxylumistrol(3) (JN), which has little ability to alter gene expression and also because a nongenomic antagonist of 1,25(OH)(2)D(3) abolished protection. In the current study, we tested whether this photoprotective effect would extend to other types of DNA damage, and whether this could be demonstrated in human ex vivo skin, as this model would be suited to pre-clinical testing of topical formulations for photoprotection. In particular, using skin explants, we examined a time course for thymine dimers (TD), the most abundant DNA photolesion, as well as 8 - oxo-7,8-dihydro-2'-deoxyguanosine ( 8 - oxodG), which is a mutagenic DNA base lesion arising from UV-induced oxidative stress, and 8 - nitroguanosine ( 8-NG). Nitric oxide products, known markers for chronic inflammation and carcinogenesis, are also induced by UV.
This study showed that 1,25(OH)(2)D(3) significantly reduced TD and 8-NG as early as 30 minutes post UV, and 8 - oxodG at 3 hours post UV, confirming the photoprotective effect of 1,25(OH)(2)D(3) against DNA photoproducts in human skin explants.
At least in part, the mechanism of photoprotection by 1,25(OH)(2)D(3) is likely to be through the reduction of reactive nitrogen species and the subsequent reduction in oxidative and nitrosative damage.
Copyright © 2012. Published by Elsevier Ltd, PMID: 23165145
International Journal of Molecular Sciences, www.mdpi.com/journal/ijms
Katie M. Dixon 1,2,% Wannit Tongkao-On 1, Vanessa B. Sequeira 1, Sally E. Carter 1, Eric J. Song 1, Mark S. Rybchyn 1, Clare Gordon-Thomson 1 and Rebecca S. Mason 1
1 Discipline of Physiology, Bosch Institute, School of Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia; E-Mails: wton9162 at uni.sydney.edu.au (W.T.-O.); vanessa at physiol.usyd.edu.au (V.B.S.); scar1097 at uni.sydney.edu.au (S.E.C.); eson8487 at uni.sydney.edu.au (E.J.S.); mrybchyn at mail.usyd.edu.au (M.S.R.); claregt at physiol.usyd.edu.au (C.G.-T.); rebecca.mason at sydney.edu.au (R.S.M.)
2 Discipline of Anatomy and Histology, Bosch Institute, School of Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia
* Author to whom correspondence should be addressed; E-Mail: katie.dixon at sydney.edu.au; Tel.: +61-2-9351-4633 (ext. 14633); Fax: +61-2-9351-2510.
Received: 6 December 2012; in revised form: 4 January 2013 /Accepted: 10 January 2013 / Published: 18 January 2013
Exposure to sunlight is the major cause of skin cancer. Ultraviolet radiation (UV) from the sun causes damage to DNA by direct absorption and can cause skin cell death. UV also causes production of reactive oxygen species that may interact with DNA to indirectly cause oxidative DNA damage. UV increases accumulation of p53 in skin cells, which upregulates repair genes but promotes death of irreparably damaged cells. A benefit of sunlight is vitamin D, which is formed following exposure of 7-dehydrocholesterol in skin cells to UV. The relatively inert vitamin D is metabolized to various biologically active compounds, including 1,25-dihydroxyvitamin D3. Therapeutic use of vitamin D compounds has proven beneficial in several cancer types, but more recently these compounds have been shown to prevent UV-induced cell death and DNA damage in human skin cells. Here, we discuss the effects of vitamin D compounds in skin cells that have been exposed to UV. Specifically, we examine the various signaling pathways involved in the vitamin D-induced protection of skin cells from UV.
Image B = Far less damage if have lots of vitamin D
PDF is attached at the bottom of this page
Biologically efficient solar radiation: Vitamin D production and induction of cutaneous malignant melanoma
Mantas Grigalavicius, Asta Juzeniene*, Zivile Baturaite, Arne Dahlback, Johan Moan
Solar ultraviolet (UV) radiation is the main source of vitamin D production and is also the most important environmental risk factor for cutaneous malignant melanoma (CMM) development. In the present study the relationships between daily or seasonal UV radiation doses and vitamin D status, dietary vitamin D intake and CMM incidence rates at different geographical latitudes were investigated. North-South gradients of 25-hydroxyvitamin D (25(OH)D) generation and CMM induction were calculated, based on known action spectra, and compared with measured vitamin D levels and incidence rates of CMM. The relative roles of UVA and UVB in CMM induction are discussed. Latitudinal dependencies of serum 25(OH)D levels and CMM incidence rates can only partly be explained by ambient UV doses. The UV sensitivity is different among populations with different skin color. This is well known for CMM, but seems also to be true for vitamin D status. The fact that UV-induced vitamin D may reduce the risk of CMM complicates the discussion. To some extent high dietary vitamin D intake seems to compensate low UV doses.
PDF is attached at the bottom of this page
- All items in category UV and Vitamin D
- All items in category Skin and Vitamin D
- More sun skin damage if vitamin D less than 20 ng – Sept 2012
- Hypothesis – Increasing Folate or vitamin D decreases probability of skin cancer – July 2012
- Hypothesis: vitamin D suppresses skin cancer – Sept 2012
- Overview Suntans melanoma and vitamin D
- Do You need a Suncation or just vitamin D - Nov 2012
- Possible DNA damage of skin if vitamin D levels less than 20 nanograms – April 2012
- Melanoma not as thick if recently had a sunny vacation – Nov 2013
- Skin cancer (in mice) due to UV was prevented by vitamin D (active, topical) – June 2016
- UVA causes skin cancer, perhaps UVB (Vitamin D) prevents skin cancer – Jan 2017
- Sunburning reduced by 200,000 IU of Vitamin D – RCT April 2017
- Oxidative stress to DNA prevented by Vitamin D (H2O2, rats) – Jan 2019Vitamin D protects DNA against UV skin damage – 5 studies 2012-2013
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