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UVB-Induced Inflammatory Cytokine Release, DNA Damage and Apoptosis of Human Oral Compared with Skin Tissue Equivalents†
Article first published online: 29 JAN 2013
© 2013 Wiley Periodicals, Inc. Photochemistry and Photobiology © 2013 The American Society of Photobiology
Photochemistry and Photobiology
Volume 89, Issue 3, pages 665–670, May/June 2013
How to Cite
Breger, J., Baeva, L., Agrawal, A., Shindell, E. and Godar, D. E. (2013), UVB-Induced Inflammatory Cytokine Release, DNA Damage and Apoptosis of Human Oral Compared with Skin Tissue Equivalents. Photochemistry and Photobiology, 89: 665–670. doi: 10.1111/php.12030
- Issue published online: 24 APR 2013
- Article first published online: 29 JAN 2013
- Accepted manuscript online: 15 DEC 2012 09:08AM EST
- Manuscript Accepted: 3 DEC 2012
- Manuscript Received: 14 AUG 2012
- FDA's Critical Path Initiative
People can get oral cancers from UV (290–400 nm) exposures. Besides high outdoor UV exposures, high indoor UV exposures to oral tissues can occur when consumers use UV-emitting tanning devices to either tan or whiten their teeth. We compared the carcinogenic risks of skin to oral tissue cells after UVB (290–320 nm) exposures using commercially available 3D-engineered models for human skin (EpiDerm™), gingival (EpiGing™) and oral (EpiOral™) tissues. To compare the relative carcinogenic risks, we investigated the release of cytokines, initial DNA damage in the form of cyclobutane pyrimidine dimers (CPDs), repair of CPDs and apoptotic cell numbers. We measured cytokine release using cytometric beads with flow cytometry and previously developed a fluorescent immunohistochemical assay to quantify simultaneously CPD repair rates and apoptotic cell numbers. We found that interleukin-8 (IL-8) release and the initial CPDs are significantly higher, whereas the CPD repair rates and apoptotic cell numbers are significantly lower for oral compared with skin tissue cells. Thus, the increased release of the inflammatory cytokine IL-8 along with inefficient CPD repair and decreased death rates for oral compared with skin tissue cells suggests that mutations are accumulating in the surviving population of oral cells increasing people's risks for getting oral cancers.