Abstract
We previously shown that inflammatory response induced by ultraviolet B (UVB)/reactive oxygen species/DNA damage has a pivotal role for skin tumor development. It has known that some drugs as chlorothiazide induced photo-sensitivity reactions. Recently there have been reports that squamous cell carcinoma in sun exposed areas developed after administration of voriconazole, anti-fungal agent. We studied the effects of inflammatory response with or without voriconazole using xeroderma pigmentosum complementation group A model mice (Xpa-deficient mice). Skin carcinogenesis by repetitive UVB exposure with voriconazole on Xpa-deficient mice were also investigated. We compared the serum level of cytokines from Xpa-deficient mice irradiated by UVB or UVA and administered with voriconazole, chlorothiazide and vehicle control by cytokine array assay. We exposed UVB on the groups of each drug administered along with wild-type mice twice a week for 10 weeks-UVB exposure for the evaluation of skin tumor development. The serum of Xpa-deficient mice of voriconazole or chlorothiazide and UVB significantly elevated wide variety of cytokines compared with vehicle only administration. Both agents increase the expression of CXCLl1, M-CSF, CCL2, CCL12, CXCL12, TNFα, GCSF and IL16 after UVB exposure, furthermore, the serum of voriconazole plus UVB exposure up-regulated exclusively the level of IFN-γ, IL1α, IL1β, IL4, IL7, IL13 and CCL9. Chronic UVB exposure on Xpa-deficient mice with voriconazole administration significantly showed much more tumors, tumor volumes and faster induction compared with vehicle group. The mechanism of skin tumor development in sun-exposed area after administration of voriconazole indicates that voriconazole induced strong inflammatory response following DNA damage by UVB.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
