Nicotinamide enhances repair of arsenic and ultraviolet radiation-induced DNA damage in HaCaT keratinocytes and ex vivo human skin

Arsenic-induced skin cancer is a significant global health burden. In areas with arsenic contamination of water sources, such as China, Pakistan, Myanmar, Cambodia and especially Bangladesh and West Bengal, large populations are at risk of arsenic-induced skin cancer. Arsenic acts as a co-carcinogen...

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Veröffentlicht in:PloS one 2015-02, Vol.10 (2), p.e0117491
Hauptverfasser: Thompson, Benjamin C, Halliday, Gary M, Damian, Diona L
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description Arsenic-induced skin cancer is a significant global health burden. In areas with arsenic contamination of water sources, such as China, Pakistan, Myanmar, Cambodia and especially Bangladesh and West Bengal, large populations are at risk of arsenic-induced skin cancer. Arsenic acts as a co-carcinogen with ultraviolet (UV) radiation and affects DNA damage and repair. Nicotinamide (vitamin B3) reduces premalignant keratoses in sun-damaged skin, likely by prevention of UV-induced cellular energy depletion and enhancement of DNA repair. We investigated whether nicotinamide modifies DNA repair following exposure to UV radiation and sodium arsenite. HaCaT keratinocytes and ex vivo human skin were exposed to 2μM sodium arsenite and low dose (2J/cm2) solar-simulated UV, with and without nicotinamide supplementation. DNA photolesions in the form of 8-oxo-7,8-dihydro-2'-deoxyguanosine and cyclobutane pyrimidine dimers were detected by immunofluorescence. Arsenic exposure significantly increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine in irradiated cells. Nicotinamide reduced both types of photolesions in HaCaT keratinocytes and in ex vivo human skin, likely by enhancing DNA repair. These results demonstrate a reduction of two different photolesions over time in two different models in UV and arsenic exposed cells. Nicotinamide is a nontoxic, inexpensive agent with potential for chemoprevention of arsenic induced skin cancer.
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Peter</contributor><creatorcontrib>Thompson, Benjamin C ; Halliday, Gary M ; Damian, Diona L ; Soyer, H. Peter</creatorcontrib><description>Arsenic-induced skin cancer is a significant global health burden. In areas with arsenic contamination of water sources, such as China, Pakistan, Myanmar, Cambodia and especially Bangladesh and West Bengal, large populations are at risk of arsenic-induced skin cancer. Arsenic acts as a co-carcinogen with ultraviolet (UV) radiation and affects DNA damage and repair. Nicotinamide (vitamin B3) reduces premalignant keratoses in sun-damaged skin, likely by prevention of UV-induced cellular energy depletion and enhancement of DNA repair. We investigated whether nicotinamide modifies DNA repair following exposure to UV radiation and sodium arsenite. HaCaT keratinocytes and ex vivo human skin were exposed to 2μM sodium arsenite and low dose (2J/cm2) solar-simulated UV, with and without nicotinamide supplementation. DNA photolesions in the form of 8-oxo-7,8-dihydro-2'-deoxyguanosine and cyclobutane pyrimidine dimers were detected by immunofluorescence. Arsenic exposure significantly increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine in irradiated cells. Nicotinamide reduced both types of photolesions in HaCaT keratinocytes and in ex vivo human skin, likely by enhancing DNA repair. These results demonstrate a reduction of two different photolesions over time in two different models in UV and arsenic exposed cells. 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Peter</contributor><creatorcontrib>Thompson, Benjamin C</creatorcontrib><creatorcontrib>Halliday, Gary M</creatorcontrib><creatorcontrib>Damian, Diona L</creatorcontrib><title>Nicotinamide enhances repair of arsenic and ultraviolet radiation-induced DNA damage in HaCaT keratinocytes and ex vivo human skin</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Arsenic-induced skin cancer is a significant global health burden. In areas with arsenic contamination of water sources, such as China, Pakistan, Myanmar, Cambodia and especially Bangladesh and West Bengal, large populations are at risk of arsenic-induced skin cancer. Arsenic acts as a co-carcinogen with ultraviolet (UV) radiation and affects DNA damage and repair. Nicotinamide (vitamin B3) reduces premalignant keratoses in sun-damaged skin, likely by prevention of UV-induced cellular energy depletion and enhancement of DNA repair. 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Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nicotinamide enhances repair of arsenic and ultraviolet radiation-induced DNA damage in HaCaT keratinocytes and ex vivo human skin</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-02-06</date><risdate>2015</risdate><volume>10</volume><issue>2</issue><spage>e0117491</spage><pages>e0117491-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Arsenic-induced skin cancer is a significant global health burden. In areas with arsenic contamination of water sources, such as China, Pakistan, Myanmar, Cambodia and especially Bangladesh and West Bengal, large populations are at risk of arsenic-induced skin cancer. Arsenic acts as a co-carcinogen with ultraviolet (UV) radiation and affects DNA damage and repair. Nicotinamide (vitamin B3) reduces premalignant keratoses in sun-damaged skin, likely by prevention of UV-induced cellular energy depletion and enhancement of DNA repair. We investigated whether nicotinamide modifies DNA repair following exposure to UV radiation and sodium arsenite. HaCaT keratinocytes and ex vivo human skin were exposed to 2μM sodium arsenite and low dose (2J/cm2) solar-simulated UV, with and without nicotinamide supplementation. DNA photolesions in the form of 8-oxo-7,8-dihydro-2'-deoxyguanosine and cyclobutane pyrimidine dimers were detected by immunofluorescence. Arsenic exposure significantly increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine in irradiated cells. Nicotinamide reduced both types of photolesions in HaCaT keratinocytes and in ex vivo human skin, likely by enhancing DNA repair. These results demonstrate a reduction of two different photolesions over time in two different models in UV and arsenic exposed cells. Nicotinamide is a nontoxic, inexpensive agent with potential for chemoprevention of arsenic induced skin cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25658450</pmid><doi>10.1371/journal.pone.0117491</doi><tpages>e0117491</tpages><oa>free_for_read</oa></addata></record>
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subjects Arsenic
Arsenic compounds
Arsenite
Arsenites - pharmacology
Cancer
Carcinogens
Cell Line
Chemotherapy
Computer simulation
Contamination
Cyclobutane
Cyclobutane pyrimidine dimers
Damage prevention
Deoxyguanosine
Deoxyribonucleic acid
Dimers
DNA
DNA damage
DNA Damage - drug effects
DNA Damage - radiation effects
DNA repair
DNA Repair - drug effects
Exposure
Global health
Health risks
Humans
Immunofluorescence
Keratinocytes
Keratinocytes - drug effects
Keratinocytes - radiation effects
Niacinamide
Niacinamide - pharmacology
Nicotinamide
Nicotinic acid
Radiation damage
Radiation effects
Repair
Skin
Skin - drug effects
Skin - radiation effects
Skin cancer
Skin diseases
Sodium
Sodium arsenite
Sodium Compounds - pharmacology
Supplements
Ultraviolet radiation
Ultraviolet Rays
Water pollution
Water sources
Wound Healing - drug effects
title Nicotinamide enhances repair of arsenic and ultraviolet radiation-induced DNA damage in HaCaT keratinocytes and ex vivo human skin
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