{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T17:25:39Z","timestamp":1791134739300,"version":"4.1.0"},"reference-count":60,"publisher":"National Academy of Sciences","issue":"48","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2009,12]]},"abstract":"<jats:p>\n                    Cystic fibrosis (CF) is a pleiotropic disease, originating from mutations in the CF transmembrane conductance regulator (CFTR). Lung injuries inflicted by recurring infection and excessive inflammation cause \u224890% of the morbidity and mortality of CF patients. It remains unclear how CFTR mutations lead to lung illness. Although commonly known as a Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    channel, CFTR also conducts thiocyanate (SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    ) ions, important because, in several ways, they can limit potentially harmful accumulations of hydrogen peroxide (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ) and hypochlorite (OCl\n                    <jats:sup>\u2212<\/jats:sup>\n                    ). First, lactoperoxidase (LPO) in the airways catalyzes oxidation of SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    to tissue-innocuous hypothiocyanite (OSCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    ), while consuming H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . Second, SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    even at low concentrations competes effectively with Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    for myeloperoxidase (MPO) (which is released by white blood cells), thus limiting OCl\n                    <jats:sup>\u2212<\/jats:sup>\n                    production by the enzyme. Third, SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    can rapidly reduce OCl\n                    <jats:sup>\u2212<\/jats:sup>\n                    without catalysis. Here, we show that SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    and LPO protect a lung cell line from injuries caused by H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ; and that SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    protects from OCl\n                    <jats:sup>\u2212<\/jats:sup>\n                    made by MPO. Of relevance to inflammation in other diseases, we find that in three other tested cell types (arterial endothelial cells, a neuronal cell line, and a pancreatic \u03b2 cell line) SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    at concentrations of \u2265100 \u03bcM greatly attenuates the cytotoxicity of MPO. Humans naturally derive SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    from edible plants, and plasma SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    levels of the general population vary from 10 to 140 \u03bcM. Our findings raise the possibility that insufficient levels of antioxidant SCN\n                    <jats:sup>\u2212<\/jats:sup>\n                    provide inadequate protection from OCl\n                    <jats:sup>\u2212<\/jats:sup>\n                    , thus worsening inflammatory diseases, and predisposing humans to diseases linked to MPO activity, including atherosclerosis, neurodegeneration, and certain cancers.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0911412106","type":"journal-article","created":{"date-parts":[[2009,11,16]],"date-time":"2009-11-16T22:24:45Z","timestamp":1258410285000},"page":"20515-20519","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":125,"title":["The antioxidant role of thiocyanate in the pathogenesis of cystic fibrosis and other inflammation-related diseases"],"prefix":"10.1073","volume":"106","author":[{"given":"Yanping","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Physiology, Howard Hughes Medical Institute, University of Pennsylvania, 3700 Hamilton Walk, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Szilvia","family":"Sz\u00e9p","sequence":"additional","affiliation":[{"name":"Department of Physiology, Howard Hughes Medical Institute, University of Pennsylvania, 3700 Hamilton Walk, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhe","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Physiology, Howard Hughes Medical Institute, University of Pennsylvania, 3700 Hamilton Walk, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2009,12]]},"reference":[{"key":"e_1_3_3_1_2","first-page":"303","article-title":"Quantitative evaluation of the development of tracheal submucosal glands in infants with cystic fibrosis and control infants","volume":"106","author":"Sturgess J","year":"1982","unstructured":"J Sturgess, J Imrie, Quantitative evaluation of the development of tracheal submucosal glands in infants with cystic fibrosis and control infants. 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