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NUCLEOTIDE EXCISION REPAIR IS REDUCED IN ORAL EPITHELIAL TISSUES COMPARED WITH SKIN.

Mitchell1, D., Paniker1, L. and Godar2, D. 1Department of Carcinogenesis, University of Texas, MD Anderson Cancer Center, Smithville, TX. 2US Food and Drug Administration, Center for Devices and Radiological Health, Silver Spring, MD.
Abstract

Ultraviolet radiation (UVR) exposure to internal tissues for diagnostic, therapeutic and cosmetic procedures has increased dramatically over the past decade. The greatest increase in UVR exposure of internal tissues occurs in the cosmetic industry where it is combined with oxidizing agents for teeth whitening, often in conjunction with indoor tanning. To address potential carcinogenic risks of these procedures, we analyzed the formation and repair of the DNA photoproducts associated with the signature mutations of UVR. Radioimmunoassay was used to quantify the induction and repair of cyclobutane pyrimidine dimers and pyrimidine(6-4)pyrimidone photoproducts in DNA purified from three reconstructed tissues, EpiDerm™, EpiGingival™ and EpiOral™. We observed comparable levels of DNA damage in all tissues immediately after UVR exposure. In contrast, repair was significantly reduced in both oral tissues compared with EpiDerm™. Our data suggest that UVR exposure of oral tissues can result in accumulation of DNA damage and increase the risk for carcinoma and melanoma of the mouth. Because NER is a broad-spectrum defense against DNA damage caused by a variety of agents in addition to UVR, our data suggest that the relatively low NER efficiency observed in oral tissues may have wide-ranging consequences in this highly exposed environment.

Keywords

Nucleotide excision repair, carcinogenic risks, DNA photoproducts, cyclobutane pyrimidine dimmers, pyrimidine(6-4)pyrimidone photoproducts, EpiDerm (EPI-200), EpiGingival (Gin-100), EpiOral (ORL-200), Oral squamous cell carcinoma

Materials Tested

Ultraviolet radiation (UVR), UVA, UVB

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