{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T06:57:07Z","timestamp":1793429827822,"version":"4.5.0"},"reference-count":33,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2008,4,1]],"date-time":"2008-04-01T00:00:00Z","timestamp":1207008000000},"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":["Hum Exp Toxicol"],"published-print":{"date-parts":[[2008,4]]},"abstract":"<jats:p>\n                    Siderosis bulbi is vision threatening. An investigation into its mechanisms and management is crucial. Experimental siderosis was established by intravitreous administration of an iron particle (chronic) or FeSO\n                    <jats:sub>4<\/jats:sub>\n                    (acute). After siderosis, there was a significant dose-responsive reduction in eletroretinogram (a\/b-wave) amplitude, and an increase in\n                    <jats:sup>\n                      <jats:sup>\u2022<\/jats:sup>\n                    <\/jats:sup>\n                    OH level, greater when caused by 24\u00a0mM FeSO\n                    <jats:sub>4<\/jats:sub>\n                    than that by 8\u00a0mM FeSO\n                    <jats:sub>4<\/jats:sub>\n                    . Furthermore, the FeSO\n                    <jats:sub>4<\/jats:sub>\n                    -induced oxidative stress was significantly blunted by 100\u00a0\u03bcM ferulic acid (FA). Siderosis also resulted in an excessive glutamate release, increased [Ca\n                    <jats:sup>++<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    , and enhanced superoxide dismutase immunoreactivity. The latter finding was consistent with the Western blot result. Obvious disorganization including loss of photoreceptor outer segments and cholinergic amacrines together with a wide-spreading ferric distribution across the retina was present, which were related to the eletro-retinographic and pathologic dysfunctions. Furthermore, b-wave reduction and amacrine damage were respectively, significantly, dose-dependently, and clearly ameliorated by FA. Thus, siderosis stimulates oxidative stress, and possibly, subsequent excitotoxicity, and calcium influx, which explains why the retina is impaired electro-physiologically and pathologically. Importantly, FA protects iron toxicity perhaps by acting as a free radical scavenger. This provides an approach to the study and treatment of the iron-related disorders such as retained intraocular iron and Alzheimer disease.\n                  <\/jats:p>","DOI":"10.1177\/0960327108092294","type":"journal-article","created":{"date-parts":[[2008,8,6]],"date-time":"2008-08-06T08:18:38Z","timestamp":1218010718000},"page":"327-339","source":"Crossref","is-referenced-by-count":22,"title":["Iron-generated hydroxyl radicals kill retinal cells in vivo: effect of ferulic acid"],"prefix":"10.1177","volume":"27","author":[{"given":"HM","family":"Chao","sequence":"first","affiliation":[{"name":"Department of Ophthalmology, Veterans General Hospital, Taipei, Taiwan, Republic of China; Department of Ophthalmology, Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China; Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China; Institute of Biomedical Engineering, National Yang-Ming University, Taipei, Taiwan, Republic of China; Department of Ophthalmology, China Medical University Hospital,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YH","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Veterans General Hospital, Taipei, Taiwan, Republic of China; Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JH","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China; Cheng Hsin Rehabilitation Medical Center, Taipei, Taiwan, Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"SM","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Veterans General Hospital, Taipei, Taiwan, Republic of China; Department of Ophthalmology, Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"FL","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Veterans General Hospital, Taipei, Taiwan, Republic of China; 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