Up-regulation of plasma membrane-associated redox activities in neuronal cells lacking functional mitochondria

Dong Hoon Hyun, Nicole D. Hunt, Scott S. Emerson, Joe O. Hernandez, Mark P. Mattson, Rafael De Cabo

Research output: Contribution to journalArticlepeer-review

59 Scopus citations


Mitochondria-deficient cells (ρo cells) survive through enhanced glycolytic metabolism in the presence of pyruvate and uridine. The plasma membrane redox system (PMRS) contains several NAD(P)H-related enzymes and plays a key role in maintaining the levels of NAD+/NADH and reduced coenzyme Q. In this study, ρo cells were used to investigate how the PMRS is regulated under conditions of mitochondrial dysfunction. ρo cells exhibited a lower oxygen consumption rate and higher levels of lactate than parental cells, and were more sensitive to glycolysis inhibitors (2-deoxyglucose and iodoacetamide) than control cells. However, they were more resistant to H2O2, consistent with increased catalase activity and decreased oxidative damage (protein carbonyls and nitrotyrosine). PM-associated redox enzyme activities were enhanced in ρo 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-regulated 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.

Original languageEnglish
Pages (from-to)1364-1374
Number of pages11
JournalJournal of Neurochemistry
Issue number5
StatePublished - Mar 2007


  • Mitochondrial deficiency
  • Oxidative stress
  • Plasma membrane redox system


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