{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T22:26:30Z","timestamp":1792016790697,"version":"4.4.0"},"reference-count":32,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2014,7,1]],"date-time":"2014-07-01T00:00:00Z","timestamp":1404172800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2014,7]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Aims:<\/jats:italic>\n                    <\/jats:bold>\n                    Systemic lupus erythematosus (SLE) patients' peripheral blood lymphocytes (PBL) show mitochondrial dysfunction and oxidative stress. To determine the electrochemical bases of mitochondrial dysfunction, we measured electron transport chain (ETC) activity and its regulation by\n                    <jats:italic toggle=\"yes\">N<\/jats:italic>\n                    -acetylcysteine (NAC) that reversed glutathione depletion and improved disease activity in SLE. ETC activity was assessed in PBL of 69 SLE patients and 37 healthy donors. Negatively isolated T cells were examined in 7 SLE patients, 11 healthy donors, and 10 nonlupus inflammatory arthritis (IA) donors.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Results:<\/jats:italic>\n                    <\/jats:bold>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    consumption (in nmol\/ml\/min) by lupus PBL was increased at baseline (SLE: 2.492\u00b10.196, control: 2.137\u00b10.153;\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.027) and with complex IV substrates (SLE: 7.722\u00b10.419, control: 7.006\u00b10.505;\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.028). SLE PBL consumed more O\n                    <jats:sub>2<\/jats:sub>\n                    upon in-chamber T-cell activation (\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.012). After overnight T-cell stimulation, ETC activity of SLE PBL was 2.27-fold increased through complex I (SLE: 1.606\u00b10.273, control: 0.709\u00b10.169;\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.001) and, to a lesser extent, through complex IV. Likewise, complex I activity was elevated in negatively isolated \u201cuntouched\u201d T cells of SLE patients (1.816\u00b10.180) relative to healthy controls (0.917\u00b10.094;\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.0003) and IA disease controls studied in parallel (1.057\u00b10.199;\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.0308). NAC diminished O\n                    <jats:sub>2<\/jats:sub>\n                    consumption through complex I and H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    levels both in SLE and in control PBL.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Innovation:<\/jats:italic>\n                    <\/jats:bold>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    consumption was found to be increased in SLE patients' PBL relative to control subjects evaluated in parallel. ETC complex I is identified as the main source of oxidative stress in SLE.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Conclusions:<\/jats:italic>\n                    <\/jats:bold>\n                    Lupus PBL exhibit increased O\n                    <jats:sub>2<\/jats:sub>\n                    consumption through mitochondrial ETC complex I that is inhibited by NAC, which may have therapeutic efficacy through reducing oxidative stress in SLE.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    21, 56\u201365.\n                  <\/jats:p>","DOI":"10.1089\/ars.2013.5702","type":"journal-article","created":{"date-parts":[[2014,3,27]],"date-time":"2014-03-27T11:39:08Z","timestamp":1395920348000},"page":"56-65","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":97,"title":["Increased Mitochondrial Electron Transport Chain Activity at Complex I Is Regulated by\n                    <i>N<\/i>\n                    -Acetylcysteine in Lymphocytes of Patients with Systemic Lupus Erythematosus"],"prefix":"10.1177","volume":"21","author":[{"given":"Edward","family":"Doherty","sequence":"first","affiliation":[{"name":"State University of New York"},{"name":"State University of New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zachary","family":"Oaks","sequence":"additional","affiliation":[{"name":"State University of New York"},{"name":"State University of New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andras","family":"Perl","sequence":"additional","affiliation":[{"name":"State University of New York"},{"name":"State University of New York"},{"name":"State University of New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2014,7,1]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.51.32994"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.162.3.1466"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780350606"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1136\/annrheumdis-2013-203794"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.13.7631"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1995.1311"},{"key":"e_1_3_3_8_2","unstructured":"This reference has been deleted."},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa042976"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2003.12.031"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.autrev.2008.07.041"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.22085"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0803600"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1517\/14656560902971003"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1002\/1529-0131(200201)46:1<175::AID-ART10015>3.0.CO;2-H"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.2.1092"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780400928"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M803432200"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.34502"},{"key":"e_1_3_3_20_2","first-page":"409","article-title":"Pharmacological treatment of chronic obstructive pulmonary disease","volume":"1","author":"Montuschi P","year":"2006","unstructured":"Montuschi P. Pharmacological treatment of chronic obstructive pulmonary disease. 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