Beneficial effects of UV radiation other than via vitamin D production.

Dermato-endocrinology, Apr 2012

Most of the positive effects of solar radiation are mediated via ultraviolet-B (UVB) induced production of vitamin D in skin. However, several other pathways may exist for the action of ultraviolet (UV) radiation on humans as focused on in this review. ...

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Beneficial effects of UV radiation other than via vitamin D production.

REVIEW Dermato-Endocrinology 4:2, 109–117; April/May/June 2012; G 2012 Landes Bioscience Beneficial effects of UV radiation other than via vitamin D production Asta Juzeniene1,* and Johan Moan1,2 1 Department of Radiation Biology; Institute for Cancer Research; The Norwegian Radium Hospital; Oslo University Hospital; Oslo, Norway; 2 Department of Physics; University of Oslo; Oslo, Norway . e nc Keywords: ultraviolet radiation, tanning, photoprotection, heliotherapy, phototherapy, vitamin D synthesis, nitric oxide Most of the positive effects of solar radiation are mediated via ultraviolet-B (UVB) induced production of vitamin D in skin. However, several other pathways may exist for the action of ultraviolet (UV) radiation on humans as focused on in this review. One is induction of cosmetic tanning (immediate pigment darkening, persistent pigment darkening and delayed tanning). UVB-induced, delayed tanning (increases melanin in skin after several days), acts as a sunscreen. Several human skin diseases, like psoriasis, vitiligo, atopic dermatitis and localized scleroderma, can be treated with solar radiation (heliotherapy) or artificial UV radiation (phototherapy). UV exposure can suppress the clinical symptoms of multiple sclerosis independently of vitamin D synthesis. Furthermore, UV generates nitric oxide (NO), which may reduce blood pressure and generally improve cardiovascular health. UVAinduced NO may also have antimicrobial effects and furthermore, act as a neurotransmitter. Finally, UV exposure may improve mood through the release of endorphins. higher doses of UVA exposure and persist up to several days or weeks.7,9 DT develops over 3–7 days after UVB exposure, and then remains for weeks.10 The mechanisms of UVA- and UVBinduced pigmentation are different.11 UVA induces IPD and PPD through oxidation of pre-existing melanin or melanogenic precursors.6 IPD is oxygen dependent, and reactive oxygen radicals are considered to be responsible for this process.7,12,13 PPD is also due to the upward movement of melanosomes toward the surface of the skin.10 Persons with lightest skin (skin type I) do almost not tan, while IPD and PPD are strongest in moderately and darkly pigmented skin.14,15 DT results from synthesis of melanin in the melanocytes, followed by melanin distribution to neighboring keratinocytes.6,7,10 The levels of UV radiation from the sun vary with latitude, altitude, weather, time of day and season of year. Facultative pigmentation (i.e., that induced by UV) decays during winter months at higher latitudes due to low temperatures and low UV levels. Some people want to maintain facultative tanning throughout the year for cosmetic purposes. They often use sunbeds or travel south for sunny vacations. Indoor tanning is popular, not only among Caucasians in countries with low annual UV levels (Northern countries),16,17 but also in countries with high annual UV levels (Australia).18,19 Sunbeds have several times higher UVA fluence rates than found in solar radiation under relevant conditions,19,20 and, due to this, IPD and PPD are pronounced after sunbathing. Additionally, under certain conditions UVA-induced pigmentation lasts longer than UVB-induced DP.9 This can be partly explained by the facts that UVB-induced tanning is located in the upper layers of the epidermis, while UVA-induced tanning is primary localized in the basal cell layer.11 However, high doses of UV radiation from sun or indoor tanning devices lead not only to tanning, but also to erythema, local and systemic immunosuppression, DNA damage, photoaging and photocarcinogenesis.17,21,22 e i c s o i B . e s t e u d b i n r a t L s i 2 d 1 t 0 o 2 n o © D Introduction Solar ultraviolet (UV) radiation has been used since ancient times to treat various diseases. This has a scientific background in the fact that a large number of molecules (chromophores) in different layers of the skin interact with and absorb UV. These interactions may have both positive and negative biological implications. In this review we only concentrate on the positive effects other than those directly related to vitamin D production. Cosmetic Tanning Some Africans and Asians avoid sun and use bleaching products to lighten skin, while many Caucasians seek the sun for tanning to achieve a bronze skin to “look good.”1–3 UV radiation from the sun or from artificial sources increases skin pigmentation.4,5 There are three phases of tanning: immediate pigment darkening (IPD), persistent pigment darkening (PPD) and delayed tanning (DT).6,7 IPD occurs during the first minutes of exposure to UVA, and then fades within few hours.6,8 PPD appears within hours of *Correspondence to: Asta Juzeniene; Email: Submitted: 01/24/12; Revised: 02/29/12; Accepted: 03/02/12 http://dx.doi.org/10.4161/derm.20013 www.landesbioscience.com Photoprotection UV radiation from sun and sunbeds is the main risk factor for skin cancer.23–27 Human skin adapts to chronic UV exposure by increasing melanogenesis, thickening of the horny layer, activating of antioxidant molecules, the DNA repair systems, and secretion of cytokines.28–31 Melanin provides protection of structures in and below the skin against free, UV-induced radicals. Thus, it acts as a direct shield Dermato-Endocrinology 109 from UV and visible light radiation. UV radiation causes DNA damage in the nuclei of keratinocytes, resulting in activation of p53, which transcriptionally upregulates the expression of the gene encoding proopiomelanocortin (POMC).32 The POMC precursor polypeptide is processed into several bioactive products, including a-melanocyte-stimulating hormone (a-MSH), adrenocorticotropic hormone (ACTH) and β-endorphin.32,33 After secretion, a-MSH binds to the melanocortin 1 receptor (MC1R) located on melanocytes and activates melanin production.32,33 The anti-inflammatory effects of a-MSH and ACTH may help relieve irritation and local inflammation in UV-exposed skin.33,34 Although UVA- and UVB-induced pigmentations are visually identical, only UVB-pigmentation results in a protection which is as large as corresponding to a factor of about 2 to 3 against DNA photodamage and erythema.11,35,36 This protection is equivalent to using a sunscreen with a sun protection factor (SPF) of 2 to 3.4 UVA tanning is not involved in melanin production, nor in photoprotection.7,11,36 The evolutionary role of IPD still remains unknown. Recently we have proposed that the biological role of IPD is protection of folates against photodegradation, which would be of large evolutionary importance for early hominids.37 We found that IPD had an absorption spectrum covering a number of endogenous photosensitizers in skin, such as porphyrins and riboflavin.38 UVB induces hyperkeratosis and thickening of the stratum corneum, thus reducing UV transmission.30,31,39 However, the relative importance of stratum corneum thickening and pigmentation in photoprotection is debated.30,31,39 UVA photons excite en (...truncated)


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A. Juzeniene, J. Moan. Beneficial effects of UV radiation other than via vitamin D production., Dermato-endocrinology, 2012, pp. 109, Volume 4, Issue 2, DOI: 10.4161/derm.20013