Journal
JOURNAL OF NEUROCHEMISTRY
Volume 77, Issue 3, Pages 804-811Publisher
WILEY
DOI: 10.1046/j.1471-4159.2001.00271.x
Keywords
ATP depletion; 17 beta-estradiol; mitochondrial membrane potential; 3-nitroproprionic acid; reactive oxygen species
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Funding
- NIA NIH HHS [AG 10485] Funding Source: Medline
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Mitochondria are recognized as modulators of neuronal viability during ischemia, hypoxia and toxic chemical exposure, wherein mitochondria dysfunction leading to ATP depletion may be a common pathway of cell death. Estrogens have been reported to be neuroprotective and proposed to play a role in the modulation of cerebral energy/glucose metabolism. To address the involvement of 17 beta -estradiol preservation of mitochondrial function, we examined various markers of mitochondrial activity in human SK-N-SH neuroblastoma cells exposed to 3-nitroproprionic acid (3-NPA), a succinate dehydrogenase inhibitor which uncouples oxidative phosphorylation. 3-NPA (10 mM) significantly increased ATP levels at 2 h then caused a 40% and a 50% decrease in ATP levels from baseline when treated for 12 h and 24 h, respectively. 3-NPA also induced significant increases in levels of cellular hydrogen peroxide and peroxynitrite at 2 h and a 60% decrease in mitochondrial membrane potential (MMP) at 12 h exposure. 17 beta -Estradiol (17-betaE(2)) pretreatment restored the ATP level back to 80% at 12 h of that in control cells treated with 3-NPA but without E-2, blunted the effect of 3-NPA on MMP and reactive oxygen species levels. The present study indicates that 17 beta -E-2 can preserve mitochondrial function in the face of inhibition of oxidative phosphorylation.
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