Journal
ANTIOXIDANTS & REDOX SIGNALING
Volume 8, Issue 5-6, Pages 955-965Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2006.8.955
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Activated astroglial cells produce large amounts of nitric oxide (NO) which, through the binding to soluble guanylyl cyclase, rapidly increases cyclic GMP concentrations. In addition, through the binding with the a-a(3) binuclear center of cytochrome c oxidase, NO rapidly decreases the affinity of this complex for O-2, hence reversibly inhibiting the mitochondrial electron flux and ATP synthesis. Despite promoting a profound degree of mitochondrial inhibition, astrocytes show remarkable resistance to NO and peroxynitrite, whereas neurons are highly vulnerable. Recent evidence suggests that the inhibition of mitochondrial respiration by these nitrogen-derived reactive species leads to the modulation of key regulatory steps of glucose metabolism. Thus, upregulation of glucose uptake, the stimulation of glycolysis and the activation of pentose-phosphate pathway appear to be important sites of action. The stimulation of these glucose-metabolizing pathways by NO would represent a transient attempt by the glial cells to compensate for energy impairment and oxidative stress, and thus to emerge from an otherwise pathological outcome.
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