{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T17:56:04Z","timestamp":1785779764300,"version":"3.56.0"},"reference-count":45,"publisher":"MDPI AG","issue":"8","license":[{"start":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T00:00:00Z","timestamp":1785715200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Antioxidants"],"abstract":"<jats:p>Keratinocytes are key epidermal cells that are highly susceptible to ultraviolet (UV)-induced damage, which can lead to DNA mutations and the development of malignancies. In parallel, UV radiation induces lipid peroxidation (LPO), potentially facilitating the activation of ferroptosis, a form of programmed cell death. We hypothesized that UV-mediated DNA damage, resulting in the formation of cyclobutane pyrimidine dimers (CPDs), occurs preferentially in cells with elevated LPO levels, and that mild induction of ferroptosis in proliferating keratinocytes selectively eliminates cells with high CPD levels. A human keratinocyte cell line was exposed to UVB radiation and subsequently treated with the ferroptosis inducers RSL3 and erastin. Cell death was assessed using LDH analysis, LPO was measured using the fluorescent probe BODIPY\u2122 581\/591 C11, and CPD formation was quantified by ELISA. Using different doses of UVB, we confirmed UVB irradiation simultaneously increases the cell death rate and LPO and CPDs levels in proliferating keratinocytes. Mild induction of ferroptosis in these cells led to a slight increase in the cell death rate and simultaneously to a drastic reduction in CPD levels, suggesting that there is a specific pool of cells predominantly susceptible to UVB in terms of DNA damage and LPO induction. Our findings support our hypothesis that induction of ferroptosis in proliferating keratinocytes exposed to UVB radiation preferentially eliminates cells with elevated CPD levels and may therefore serve as a protective mechanism against UV-induced carcinogenesis.<\/jats:p>","DOI":"10.3390\/antiox15080966","type":"journal-article","created":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T17:26:52Z","timestamp":1785778012000},"page":"966","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Keratinocytes with DNA Aberration Induced by UVB Become Susceptible to Ferroptosis"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5820-1804","authenticated-orcid":false,"given":"Yuliya D.","family":"Smirnova","sequence":"first","affiliation":[{"name":"Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA, 1200 Vienna, Austria"},{"name":"Laboratory of Metagenomics and Food Biotechnology, Voronezh State University of Engineering Technologies, 394036 Voronezh, Russia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philipp","family":"Sabler","sequence":"additional","affiliation":[{"name":"Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA, 1200 Vienna, Austria"},{"name":"Institute for Molecular Biotechnology, University of Natural Resources and Life Sciences, 1190 Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2759-211X","authenticated-orcid":false,"given":"Adelheid","family":"Weidinger","sequence":"additional","affiliation":[{"name":"Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA, 1200 Vienna, Austria"},{"name":"Austrian Cluster for Tissue Regeneration, 1200 Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5474-6332","authenticated-orcid":false,"given":"Johannes","family":"Grillari","sequence":"additional","affiliation":[{"name":"Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA, 1200 Vienna, Austria"},{"name":"Institute for Molecular Biotechnology, University of Natural Resources and Life Sciences, 1190 Vienna, Austria"},{"name":"Austrian Cluster for Tissue Regeneration, 1200 Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6302-530X","authenticated-orcid":false,"given":"Peter","family":"Dungel","sequence":"additional","affiliation":[{"name":"Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA, 1200 Vienna, Austria"},{"name":"Austrian Cluster for Tissue Regeneration, 1200 Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0834-4997","authenticated-orcid":false,"given":"Andrey V.","family":"Kozlov","sequence":"additional","affiliation":[{"name":"Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA, 1200 Vienna, Austria"},{"name":"Austrian Cluster for Tissue Regeneration, 1200 Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,8,3]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1009","DOI":"10.1038\/s41419-021-04284-5","article-title":"Inhibition of Keratinocyte Ferroptosis Suppresses Psoriatic Inflammation","volume":"12","author":"Shou","year":"2021","journal-title":"Cell Death Dis."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"860","DOI":"10.1042\/CS20255877","article-title":"YTHDF2 Regulates ACSL4-Dependent Ferroptosis of Keratinocytes in Diabetic Wound Healing","volume":"139","author":"Wu","year":"2025","journal-title":"Clin. 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