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      UV Radiation and the Skin

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          Abstract

          UV radiation (UV) is classified as a “complete carcinogen” because it is both a mutagen and a non-specific damaging agent and has properties of both a tumor initiator and a tumor promoter. In environmental abundance, UV is the most important modifiable risk factor for skin cancer and many other environmentally-influenced skin disorders. However, UV also benefits human health by mediating natural synthesis of vitamin D and endorphins in the skin, therefore UV has complex and mixed effects on human health. Nonetheless, excessive exposure to UV carries profound health risks, including atrophy, pigmentary changes, wrinkling and malignancy. UV is epidemiologically and molecularly linked to the three most common types of skin cancer, basal cell carcinoma, squamous cell carcinoma and malignant melanoma, which together affect more than a million Americans annually. Genetic factors also influence risk of UV-mediated skin disease. Polymorphisms of the melanocortin 1 receptor ( MC1R) gene, in particular, correlate with fairness of skin, UV sensitivity, and enhanced cancer risk. We are interested in developing UV-protective approaches based on a detailed understanding of molecular events that occur after UV exposure, focusing particularly on epidermal melanization and the role of the MC1R in genome maintenance.

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          Resurrection of vitamin D deficiency and rickets.

          Michael Holick (2006)
          The epidemic scourge of rickets in the 19th century was caused by vitamin D deficiency due to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformities, hypocalcemia, tetany, and seizures. The encouragement of sensible sun exposure and the fortification of milk with vitamin D resulted in almost complete eradication of the disease. Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status. 25(OH)D is activated in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D], which regulates calcium, phosphorus, and bone metabolism. Vitamin D deficiency has again become an epidemic in children, and rickets has become a global health issue. In addition to vitamin D deficiency, calcium deficiency and acquired and inherited disorders of vitamin D, calcium, and phosphorus metabolism cause rickets. This review summarizes the role of vitamin D in the prevention of rickets and its importance in the overall health and welfare of infants and children.
          Article 0 comments Cited 323 times – based on 0 reviews     Review now
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            Oxidative stress in the pathogenesis of skin disease.

            David R. Bickers, Mohammad Athar (2006)
            Skin is the largest body organ that serves as an important environmental interface providing a protective envelope that is crucial for homeostasis. On the other hand, the skin is a major target for toxic insult by a broad spectrum of physical (i.e. UV radiation) and chemical (xenobiotic) agents that are capable of altering its structure and function. Many environmental pollutants are either themselves oxidants or catalyze the production of reactive oxygen species (ROS) directly or indirectly. ROS are believed to activate proliferative and cell survival signaling that can alter apoptotic pathways that may be involved in the pathogenesis of a number of skin disorders including photosensitivity diseases and some types of cutaneous malignancy. ROS act largely by driving several important molecular pathways that play important roles in diverse pathologic processes including ischemia-reperfusion injury, atherosclerosis, and inflammatory responses. The skin possesses an array of defense mechanisms that interact with toxicants to obviate their deleterious effect. These include non-enzymatic and enzymatic molecules that function as potent antioxidants or oxidant-degrading systems. Unfortunately, these homeostatic defenses, although highly effective, have limited capacity and can be overwhelmed thereby leading to increased ROS in the skin that can foster the development of dermatological diseases. One approach to preventing or treating these ROS-mediated disorders is based on the administration of various antioxidants in an effort to restore homeostasis. Although many antioxidants have shown substantive efficacy in cell culture systems and in animal models of oxidant injury, unequivocal confirmation of their beneficial effects in human populations has proven elusive.
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              Incidence estimate of nonmelanoma skin cancer in the United States, 2006.

              Howard W Rogers, Martin Weinstock, Ashlynne R. Harris … (2010)
              To estimate the incidence of nonmelanoma skin cancer (NMSC) in the US population in 2006 and secondarily to indicate trends in numbers of procedures for skin cancer treatment. A descriptive analysis of population-based claims and US Census Bureau data combined with a population-based cross-sectional survey using multiple US government data sets, including the Centers for Medicare and Medicaid Services Fee-for-Service Physicians Claims databases, to calculate totals of skin cancer procedures performed for Medicare beneficiaries in 1992 and from 1996 to 2006 and related parameters. The National Ambulatory Medical Care Service database was used to estimate NMSC-related office visits. We combined these to estimate totals of new skin cancer diagnoses and affected individuals in the overall US population. The total number of procedures for skin cancer in the Medicare fee-for-service population increased by 76.9% from 1 158 298 in 1992 to 2 048 517 in 2006. The age-adjusted procedure rate per year per 100 000 beneficiaries increased from 3514 in 1992 to 6075 in 2006. From 2002 to 2006 (the years for which the databases allow procedure linkage to patient demographics and diagnoses), the number of procedures for NMSC in the Medicare population increased by 16.0%. In this period, the number of procedures per affected patient increased by 1.5%, and the number of persons with at least 1 procedure increased by 14.3%. We estimate the total number of NMSCs in the US population in 2006 at 3 507 693 and the total number of persons in the United States treated for NMSC at 2 152 500. The number of skin cancers in Medicare beneficiaries increased dramatically over the years 1992 to 2006, due mainly to an increase in the number of affected individuals. Using nationally representative databases, we provide evidence of much higher overall totals of skin cancer diagnoses and patients in the US population than previous estimates. These data give the most complete evaluation to date of the underrecognized epidemic of skin cancer in the United States.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: Molecular Diversity Preservation International (MDPI)
                ISSN (Electronic): 1422-0067
                Publication date Collection: June 2013
                Publication date (Electronic): 07 June 2013
                Volume: 14
                Issue: 6
                Pages: 12222-12248
                Affiliations
                [1 ]Graduate Center for Toxicology and the Departments of Pediatrics, Biomedical and Molecular Pharmacology and Physiology, Markey Cancer Center, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536, USA
                [2 ]Markey Cancer Center, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536, USA; E-Mail: stuart.jarrett@ 123456uky.edu
                [3 ]Graduate Center for Toxicology, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536, USA; E-Mail: aalma2@ 123456uky.edu (A.A.-O.); tim.scott@ 123456uky.edu (T.S.)
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: jdorazio@ 123456uky.edu ; Tel.: +1-859-323-6238; Fax: +1-859-257-8940.
                Article
                Publisher ID: ijms-14-12222
                DOI: 10.3390/ijms140612222
                PMC ID: 3709783
                PubMed ID: 23749111
                SO-VID: 8f81ad32-7ca1-4b1c-87f9-ff2066f7d428
                Copyright © © 2013 by the authors; licensee MDPI, Basel, Switzerland
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 25 April 2013
                Date revision received : 18 May 2013
                Date accepted : 24 May 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: ultraviolet radiation,skin,carcinogenesis,mutagenesis,pigmentation,cancer,melanin,melanocortin 1 receptor
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: ultraviolet radiation, skin, carcinogenesis, mutagenesis, pigmentation, cancer, melanin, melanocortin 1 receptor

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