| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6022643 | Neurobiology of Disease | 2012 | 13 Pages |
Abstract
⺠Mitochondrial function and redox status are impaired in a mouse model of Rett syndrome. ⺠The ratio of FAD/NADH autofluorescence is shifted toward oxidation in Mecp2â/y hippocampus. ⺠Cytosolic redox balance is more oxidizing and more vulnerable. ⺠Mitochondrial inhibition causes exaggerated redox responses. ⺠A radical scavenger improves redox homeostasis and qualifies as a potential pharmacotherapy.
Keywords
DEDTCFCCPFCSΔΨmBSOL-NMMAaCSFDTTFDRATZCA1DPI1,4-dithio-dl-threitol3-amino-1,2,4-triazoleCN−DMSOHydrogen peroxideCyanidebuthionine sulphoximineDiethyldithiocarbamic acidDiphenyleneiodoniumDIVDimethyl sulfoxidedays in vitrofetal calf serumartificial cerebrospinal fluidfalse discovery rateH2O2Mitochondrial membrane potentialCarbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone
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Authors
Emanuel GroÃer, Ursula Hirt, Oliwia A. Janc, Christiane Menzfeld, Marc Fischer, Belinda Kempkes, Steffen Vogelgesang, Till U. Manzke, Lennart Opitz, Gabriela Salinas-Riester, Michael Müller,