{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,5]],"date-time":"2026-04-05T00:47:49Z","timestamp":1775350069426,"version":"3.50.1"},"reference-count":32,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T00:00:00Z","timestamp":1366329600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001505","name":"Health Research Council of New Zealand","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001505","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000923","name":"Australian Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000923","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2013,8]]},"abstract":"<jats:p>\n                    Peroxiredoxin 2 (Prx2) is an abundant thiol protein in erythrocytes. It is oxidized readily on exposure to hydrogen peroxide (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ) and provides antioxidant protection by cycling between its reduced and disulfide\u2010bonded forms. To test whether Prx2 oxidation could occur in pathological situations where neutrophils are activated, we exposed human erythrocytes to stimulated neutrophils and measured Prx2 oxidation by immunoblotting of nonreducing gels. With phorbol myristate acetate, lipopolysaccharide or\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    Prx2 dimer increased from &lt;5% to up to 100% depending on neutrophil number and incubation time. Studies with inhibitors and myeloperoxidase\u2010deficient neutrophils showed that H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    generated by the neutrophil NADPH oxidase was responsible. Prx2 oxidation was detected at erythrocyte:neutrophil ratios found in blood and reversed over time as the oxidative burst subsided. Acidotic conditions also increased erythrocyte Prx2 oxidation. In a mouse model of endotoxemia induced by lipopolysaccharide, oxidized Prx2 increased transiently from &lt;1 to 15%, then reverted to baseline by 24 h. No increase was seen in mice lacking NADPH oxidase activity. These results indicate that erythrocyte Prx2 scavenges H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    produced during inflammation. Oxidized erythrocyte Prx2 could be a sensitive real\u2010time marker of systemic neutrophil activation and an early indicator of inflammation and oxidative stress.\u2014Bayer, S.B., Maghzal, G., Stocker, R., Hampton, M.B., Winterbourn, C.C. Neutrophil\u2010mediated oxidation of erythrocyte peroxiredoxin 2 as a potential marker of oxidative stress in inflammation. FASEBJ. 27, 3315\u20103322 (2013).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.13-227298","type":"journal-article","created":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T22:49:58Z","timestamp":1366411798000},"page":"3315-3322","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["Neutrophil\u2010mediated oxidation of erythrocyte peroxiredoxin 2 as a potential marker of oxidative stress in inflammation"],"prefix":"10.1096","volume":"27","author":[{"given":"Simone B.","family":"Bayer","sequence":"first","affiliation":[{"name":"Centre for Free Radical Research University of Otago Christchurch Christchurch New Zealand"},{"name":"Gravida National Research Centre for Growth and Development Department of Pathology University of Otago Christchurch Christchurch New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ghassan","family":"Maghzal","sequence":"additional","affiliation":[{"name":"Centre for Vascular Research School of Medical Sciences (Pathology) and Bosch Institute The University of Sydney Sydney New South Wales Australia"},{"name":"Vascular Biology Division The Victor Chang Cardiac Research Institute Darlinghurst New South Wales Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roland","family":"Stocker","sequence":"additional","affiliation":[{"name":"Centre for Vascular Research School of Medical Sciences (Pathology) and Bosch Institute The University of Sydney Sydney New South Wales Australia"},{"name":"Vascular Biology Division The Victor Chang Cardiac Research Institute Darlinghurst New South Wales Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark B.","family":"Hampton","sequence":"additional","affiliation":[{"name":"Centre for Free Radical Research University of Otago Christchurch Christchurch New Zealand"},{"name":"Gravida National Research Centre for Growth and Development Department of Pathology University of Otago Christchurch Christchurch New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christine C.","family":"Winterbourn","sequence":"additional","affiliation":[{"name":"Centre for Free Radical Research University of Otago Christchurch Christchurch New Zealand"},{"name":"Gravida National Research Centre for Growth and Development Department of Pathology University of Otago Christchurch Christchurch New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2013,4,19]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2010.3393"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1742-4658.2009.06985.x"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)55157-7"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2008.2081"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-08-2548"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-09-048728"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2005.07.002"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2009.08.022"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2007.00550.x"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2012.4827"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M700339200"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113230"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(17)32533-4"},{"key":"e_1_2_7_15_1","doi-asserted-by":"crossref","first-page":"319","DOI":"10.1007\/978-1-59745-467-4_21","volume-title":"Neutrophil Methods and Protocols","author":"Green J. 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