{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,2]],"date-time":"2025-12-02T15:22:44Z","timestamp":1764688964788},"reference-count":39,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,2,18]],"date-time":"2014-02-18T00:00:00Z","timestamp":1392681600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Environ and Mol Mutagen"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:p>DNA polymerase \u03b7 (pol \u03b7), of the Y\u2010family, is well known for its in vitro DNA lesion bypass ability. The most well\u2010characterized lesion bypassed by this polymerase is the cyclobutane pyrimidine dimer (CPD) caused by ultraviolet (UV) light. Historically, cellular and whole\u2010animal models for this area of research have been conducted using UV\u2010C (<jats:italic>\u03bb<\/jats:italic>\u2009=\u2009100\u2013280 nm) owing to its ability to generate large quantities of CPDs and also the more structurally distorting 6\u20104 photoproduct. Although UV\u2010C is useful as a laboratory tool, exposure to these wavelengths is generally very low owing to being filtered by stratospheric ozone. We are interested in the more environmentally relevant wavelength range of UV\u2010B (<jats:italic>\u03bb<\/jats:italic>\u2009=\u2009280\u2013315 nm) for its role in causing cytotoxicity and mutagenesis. We evaluated these endpoints in both a normal human fibroblast control line and a Xeroderma pigmentosum variant cell line in which the POLH gene contains a truncating point mutation, leading to a nonfunctional polymerase. We demonstrate that UV\u2010B has similar but less striking effects compared to UV\u2010C in both its cytotoxic and its mutagenic effects. Analysis of the mutation spectra after a single dose of UV\u2010B shows that a majority of mutations can be attributed to mutagenic bypass of dipyrimidine sequences. However, we do note additional types of mutations with UV\u2010B that are not previously reported after UV\u2010C exposure. We speculate that these differences are attributed to a change in the spectra of photoproduct lesions rather than other lesions caused by oxidative stress. Environ. Mol. Mutagen. 55:375\u2013384, 2014. \u00a9 2014 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/em.21857","type":"journal-article","created":{"date-parts":[[2014,2,18]],"date-time":"2014-02-18T13:43:26Z","timestamp":1392731006000},"page":"375-384","source":"Crossref","is-referenced-by-count":9,"title":["Detrimental effects of UV\u2010B radiation in a xeroderma pigmentosum\u2010variant cell line"],"prefix":"10.1002","volume":"55","author":[{"given":"Kimberly N.","family":"Herman","sequence":"first","affiliation":[{"name":"Department of Biological Sciences Environmental and Molecular Toxicology Program, North Carolina State University Raleigh North Carolina"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shannon","family":"Toffton","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences Environmental and Molecular Toxicology Program, North Carolina State University Raleigh North 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