The pyruvate dehydrogenase complex is partially inactivated during early recirculation following short-term forebrain ischemia in rats

Emad Zaidan, Kwan Fu Rex Sheu, Neil R. Sims

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    30 Citations (Scopus)

    Abstract

    The mechanisms of selective neuronal loss after short-term global ischemia remain undefined, but processes including increased proteolytic activity, impaired protein synthesis, and oxidative damage have been proposed to contribute. A decrease in activity of the pyruvate dehydrogenase complex in the dorsolateral striatum, an ischemia-susceptible region, is one change apparently differentiating this region from ischemia-resistant areas during early recirculation. To provide an insight into processes contributing to postischemic cell damage, the changes in the pyruvate dehydrogenase complex during early recirculation nave been further characterized. These studies provide clear confirmation that the activity of the pyruvate dehydrogenase complex is reduced in mitochondria from the dorsolateral striatum by 3 h of recirculation. The decrease in activity was not accompanied by a loss of antigenic sites or by changes in electrophoretic mobility of the components of the complex. A reduction in activity of the E1 component of the complex (39-42% decrease), but not the E2 and E3 components, was observed that was apparently sufficient to explain the decrease in activity of the whole complex. These results indicate that the changes in activity of the pyruvate dehydrogenase complex in the dorsolateral striatum are not due to loss or gross disruption of the constituent proteins but rather most likely reflect a selective inactivation of a specific component of the complex.

    Original languageEnglish
    Pages (from-to)233-241
    Number of pages9
    JournalJournal of Neurochemistry
    Volume70
    Issue number1
    DOIs
    Publication statusPublished - Jan 1998

    Bibliographical note

    Copyright:
    Copyright 2020 Elsevier B.V., All rights reserved.

    Keywords

    • Ischemia
    • Mitochondria
    • Neuronal death
    • Pyruvate dehydrogenase complex
    • Selective vulnerability

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