Rhonda M Brand1, John Mark Stottlemyer2, Melissa C Paglia2, Cara Donahue Carey2, Louis D Falo3. 1. Department of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Division of Gastroenterology and Hepatology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Magee Womens Research Institute, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: rmb91@pitt.edu. 2. Department of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA. 3. Department of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA; The Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, PA, USA; The McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA; The UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, USA.
Abstract
BACKGROUND: Excessive UV radiation disrupts skin homeostasis by multiple mechanisms that extend beyond the simple erythema associated with sunburns including reduction of antioxidants, increased DNA damage, and impairment of skin immune responses. Recreational UV exposure frequently occurs concurrently with excessive ethanol (EtOH). Epidemiological studies suggest a harmful, dose-dependent impact of EtOH in the setting of high UV exposure, leading to increased severity of sunburns relative to those generated in the absence of EtOH. Furthermore, EtOH consumption and UV radiation have multiple overlapping effects on the skin that could account for the epidemiological association. OBJECTIVE: To elucidate the relationship between excessive EtOH ingestion and UV exposures on early skin damage and downstream immune dysfunction. METHODS: We examined the impact of UVB on local skin damage, including inflammation, sunburned cells, apoptotic cells, melanin and antioxidant levels, DNA damage and immune dysfunction in the presence or absence of EtOH ingestion by combining standard mouse models of EtOH consumption and UVB exposure models. To confirm that the observed changes in mouse skin were relevant to human skin, we investigated the effects of EtOH on UV-induced skin damage with human skin explants. RESULTS: We demonstrated that EtOH consumption and UV exposure act synergistically to increase the severity of local skin damage resulting in impaired melanin responses, reduced antioxidants, greater DNA damage, and immune dysfunction as measured by reduced contact hypersensitivity. CONCLUSIONS: The results support incorporation of the risks of combined UV exposure and excessive alcohol consumption into public health campaigns.
BACKGROUND: Excessive UV radiation disrupts skin homeostasis by multiple mechanisms that extend beyond the simple erythema associated with sunburns including reduction of antioxidants, increased DNA damage, and impairment of skin immune responses. Recreational UV exposure frequently occurs concurrently with excessive ethanol (EtOH). Epidemiological studies suggest a harmful, dose-dependent impact of EtOH in the setting of high UV exposure, leading to increased severity of sunburns relative to those generated in the absence of EtOH. Furthermore, EtOH consumption and UV radiation have multiple overlapping effects on the skin that could account for the epidemiological association. OBJECTIVE: To elucidate the relationship between excessive EtOH ingestion and UV exposures on early skin damage and downstream immune dysfunction. METHODS: We examined the impact of UVB on local skin damage, including inflammation, sunburned cells, apoptotic cells, melanin and antioxidant levels, DNA damage and immune dysfunction in the presence or absence of EtOH ingestion by combining standard mouse models of EtOH consumption and UVB exposure models. To confirm that the observed changes in mouse skin were relevant to human skin, we investigated the effects of EtOH on UV-induced skin damage with human skin explants. RESULTS: We demonstrated that EtOH consumption and UV exposure act synergistically to increase the severity of local skin damage resulting in impaired melanin responses, reduced antioxidants, greater DNA damage, and immune dysfunction as measured by reduced contact hypersensitivity. CONCLUSIONS: The results support incorporation of the risks of combined UV exposure and excessive alcohol consumption into public health campaigns.
Authors: Daniel J Fitzgerald; Katherine A Radek; Mitchell Chaar; Douglas E Faunce; Luisa A DiPietro; Elizabeth J Kovacs Journal: Alcohol Clin Exp Res Date: 2007-02 Impact factor: 3.455
Authors: Rhonda M Brand; Michael W Epperly; J Mark Stottlemyer; Erin M Skoda; Xiang Gao; Song Li; Saiful Huq; Peter Wipf; Valerian E Kagan; Joel S Greenberger; Louis D Falo Journal: J Invest Dermatol Date: 2016-10-26 Impact factor: 8.551
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