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Dependence of Excitotoxic Neurodegeneration on Mitochondrial Aconitase Inactivation by Qing-You Li; Cynthia Pedersen; Brian J. Day; Manisha Patel is a Neuroscience article available to read on EtoBox.

What is Dependence of Excitotoxic Neurodegeneration on Mitochondrial Aconitase Inactivation about?

Using the inactivation of mitochondrial and cytosolic aconitases as markers of compartment‐specific superoxide (O~2~^−^) production, we show that oxygen‐glucose deprivation (OGD) or excitotoxin exposure produce a time‐dependent inactivation of mitochondrial, but not cytosolic, aconitase in cortical cultures. To determine if mitochondrial O~2~^−^ production was an important determinant in neuronal death resulting from OGD, metalloporphyrins with varying superoxide dismutase (SOD) activity were tested for their ability to protect against mitochondrial aconitase inactivation and cell death. OGD‐induced mitochondrial aconitase inactivation and cell death was inhibited by manganese tetrakis (4‐benzoic acid) porphyrin (MnTBAP), manganese tetrakis (__N__‐ethylpyridinium‐2‐yl) porphyrin (MnTE‐2‐PyP) and NMDA receptor antagonists. By contrast, NMDA‐ or kainate (KA)‐induced mitochondrial aconitase inactivation and cell death was inhibited by MnTBAP, but not MnTE‐2‐PyP. Moreover, both MnTBAP and MnTE‐2‐PyP penetrated mitochondrial fractions of cortical cells. These data suggest that mitochondrial aconitase inactivation closely correlates with subsequent neuronal death following excitotoxicity

Who reads Dependence of Excitotoxic Neurodegeneration on Mitochondrial Aconitase Inactivation?

Author

Qing-You Li; Cynthia Pedersen; Brian J. Day; Manisha Patel

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

2001

Language

EN

Field

Neuroscience (Life Sciences)