{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T01:03:56Z","timestamp":1789434236783,"version":"build-2803163510"},"reference-count":24,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T00:00:00Z","timestamp":1789344000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T00:00:00Z","timestamp":1789344000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100011789","name":"Department of Science and Technology of Jilin Province","doi-asserted-by":"publisher","award":["YDZJ202401668ZYTS"],"award-info":[{"award-number":["YDZJ202401668ZYTS"]}],"id":[{"id":"10.13039\/501100011789","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Applied Toxicology"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Perfluorooctane sulfonic acid (PFOS) is one of the per\u2010 and polyfluoroalkyl substances (PFASs) that increases the risk of developing cardiovascular diseases (CVDs) closely related to endothelial damage. Ferroptosis is a new form of cell death involving multiple metabolic pathways; the role of ferroptosis in endothelial damage by PFOS is unknown. To investigate whether oxidative stress and ferroptosis mediate PFOS\u2010triggered endothelial injury, human umbilical vein endothelial cells (HUVECs) were exposed to PFOS with or without Fer\u20101 intervention. Cellular function was evaluated via cell viability and migration assays. Markers associated with oxidative stress and ferroptosis were quantitatively detected, and the expression of relevant proteins was further analyzed using Western blot and immunofluorescence staining. Exposure to PFOS led to elevated reactive oxygen species (ROS), Fe\n                    <jats:sup>2+<\/jats:sup>\n                    accumulation, malondialdehyde (MDA) levels, and reduced glutathione (GSH) and glutathione peroxidase 4 (GPX4) expression. These changes were accompanied by impaired cell migration and alterations in endothelial function\u2010related indicators and vasoactive mediators. Fer\u20101 intervention partially attenuated PFOS\u2010induced impairment. Further mechanistic analysis showed that PFOS triggered ferroptosis through inhibiting the SLC7A11\u2013GSH\u2013GPX4 pathway and stimulating oxidative stress signal cascades.\n                  <\/jats:p>","DOI":"10.1002\/jat.70443","type":"journal-article","created":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T00:36:40Z","timestamp":1789432600000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ferroptosis and Oxidative Stress Are Implicated Perfluorooctane Sulfonate\u2010Elicited Cytotoxicity to Human Umbilical Vein Endothelial Cells"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3368-4122","authenticated-orcid":false,"given":"Jiajing","family":"Cui","sequence":"first","affiliation":[{"name":"Department of Occupational and Environmental Health, School of Public Health Jilin University  Changchun China"},{"name":"Department of Occupational Health and Environmental Health, School of 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