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The plasma membrane redox system (PMRS) contains several NAD(P)H\u2010related enzymes and plays a key role in maintaining the levels of NAD<jats:sup>+<\/jats:sup>\/NADH and reduced coenzyme Q. In this study, \u03c1<jats:sup>o<\/jats:sup> cells were used to investigate how the PMRS is regulated under conditions of mitochondrial dysfunction. \u03c1<jats:sup>o<\/jats:sup> cells exhibited a lower oxygen consumption rate and higher levels of lactate than parental cells, and were more sensitive to glycolysis inhibitors (2\u2010deoxyglucose and iodoacetamide) than control cells. However, they were more resistant to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, consistent with increased catalase activity and decreased oxidative damage (protein carbonyls and nitrotyrosine). PM\u2010associated redox enzyme activities were enhanced in \u03c1<jats:sup>o<\/jats:sup> cells compared to those in control cells. Our data suggest that all PMRS enzymes and biomarkers tested are closely related to the ability of the PMs to maintain redox homeostasis. These results illustrate that an up\u2010regulated PM redox activity can protect cells from oxidative stress as a result of an improved antioxidant capacity, and suggest a mechanism by which neurons adapt to conditions of impaired mitochondrial function.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2006.04411.x","type":"journal-article","created":{"date-parts":[[2007,1,23]],"date-time":"2007-01-23T11:43:55Z","timestamp":1169552635000},"page":"1364-1374","source":"Crossref","is-referenced-by-count":57,"title":["Up\u2010regulation of plasma membrane\u2010associated redox activities in neuronal cells lacking functional mitochondria"],"prefix":"10.1111","volume":"100","author":[{"given":"Dong\u2010Hoon","family":"Hyun","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicole D.","family":"Hunt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Scott S.","family":"Emerson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joe O.","family":"Hernandez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark P.","family":"Mattson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rafael de","family":"Cabo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,12,14]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(84)05016-3"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(91)90146-8"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M211981200"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1997.0461"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1023\/A:1022462111175"},{"key":"e_1_2_7_7_1","doi-asserted-by":"crossref","first-page":"381","DOI":"10.1023\/B:JOBB.0000041772.74810.92","article-title":"Mitochondrial dysfunction and oxidative damage in Alzheimer\u2019s and Parkinson\u2019s diseases and coenzyme Q10 as a potential treatment","volume":"36","author":"Beal M. 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