{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T21:18:11Z","timestamp":1790716691073,"version":"4.1.0"},"reference-count":18,"publisher":"SAGE Publications","issue":"5-6","license":[{"start":{"date-parts":[[2005,6,1]],"date-time":"2005-06-01T00:00:00Z","timestamp":1117584000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Toxicol Ind Health"],"published-print":{"date-parts":[[2005,6]]},"abstract":"<jats:p> Retinyl palmitate (RP) is an ester of retinol (vitamin A) and the predominant form of retinol found endogenously in the skin. We have previously reported that photoirradiation of RP with UVA light resulted in the formation of anhydroretinol (AR), 5,6-epoxyretinyl palmitate (5,6-epoxy-RP) and other photodecomposition products. While AR was formed through an ionic photodissociation mechanism, 5,6-epoxy-RP was formed through a light-mediated, free radical-initiated chain reaction. In the current study, the phototoxicity of RP, AR and 5,6-epoxy-RP in human skin Jurkat T-cells with and without light irradiation was determined using a fluorescein diacetate assay. Under similar conditions, the Comet assay was used to assess damage to cellular DNA. Nuclear DNA was not significantly damaged when the cells were irradiated by UVA plus visible light in the absence of a retinoid; however, when the cells were illuminated with UVA plus visible light in the presence of either RP, 5,6-epoxy-RP or AR (50, 100, 150 and 200 mM), DNA fragmentation was observed. Cell death was observed for retinoid concentrations of 100 mM or higher. When treated with 150 mM of RP, 5,6-epoxy-RP or AR, cell death was 52, 33 and 52%, respectively. These results suggest that RP and its two photodecomposition products, AR and 5,6-epoxy-RP, induce DNA damage and cytotoxicity when irradiated with UVA plus visible light. We also determined that photoirradiation of RP, AR and 5,6-epoxy-RP causes single strand breaks in supercoiled FX174 plasmid DNA. Using a constant dose of UVA light (50 J\/cm<jats:sup>2<\/jats:sup>), the level of DNA cleavage was highest in the presence of AR, followed by 5,6-epoxy-RP, then RP. The induced DNA strand cleavage was inhibited by NaN<jats:sub>3<\/jats:sub>. These results suggest that photoirradiation of RP, 5,6-epoxy-RP and AR with UVA light generates free radicals that initiate DNA strand cleavage. <\/jats:p>","DOI":"10.1191\/0748233705th225oa","type":"journal-article","created":{"date-parts":[[2005,7,9]],"date-time":"2005-07-09T09:57:00Z","timestamp":1120903020000},"page":"167-175","source":"Crossref","is-referenced-by-count":28,"title":["Photo-induced DNA damage and photocytotoxicity of retinyl palmitate and its photodecomposition products"],"prefix":"10.1177","volume":"21","author":[{"given":"Jian","family":"Yan","sequence":"first","affiliation":[{"name":"National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA, Department of Chemistry, Jackson State University, Jackson, MS, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingsu","family":"Xia","sequence":"additional","affiliation":[{"name":"National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shu-Hui","family":"Cherng","sequence":"additional","affiliation":[{"name":"National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA, Department of Food Science and Nutrition, Hung Kuang University, Sha-lu, Taichung, Taiwan, ROC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wayne G","family":"Wamer","sequence":"additional","affiliation":[{"name":"Center for Food Safety and Applied Nutrition, US Food and Drug Administration, College Park, MD, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul C","family":"Howard","sequence":"additional","affiliation":[{"name":"National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongtao","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Chemistry, Jackson State University, Jackson, MS, USA,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter P","family":"Fu","sequence":"additional","affiliation":[{"name":"National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2005,6,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2004.01.001"},{"key":"atypb2","first-page":"4505","volume":"53","author":"Basu-Modak, S.","year":"1993","journal-title":"Cancer Research"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1023\/A:1018941016563"},{"key":"atypb4","doi-asserted-by":"publisher","DOI":"10.1021\/tx049807l"},{"key":"atypb5","unstructured":"Cosmetic, Toiletry and Fragrance Association; Wenninger, J., Canterbery, R. 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