Journal
MITOCHONDRION
Volume 5, Issue 1, Pages 55-65Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2004.11.001
Keywords
ROS; spectrofluorometry; permeability transition; calcium uniporter; excitotoxicity; neurodegeneration
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Funding
- NINDS NIH HHS [NS34138] Funding Source: Medline
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Emerging evidence suggests that Zn2+ may impair neuronal metabolism. We examined how Zn2+ affects the activity of isolated brain mitochondria fueled with glutamate + malate, succinate or glycerol 3-phosphate. Submicromolar levels of Zn2+ dissipated membrane potential and inhibited oxygen utilization in all three substrate conditions. Zn2+-induced depolarization was reversed by the membrane-impermeant metal chelator, EGTA, and was inhibited by uniporter blockade. Cyclosporin A did not block Zn2+-induced depolarization. Added Zn2+ increased accumulation of reactive oxygen species (ROS) in glutamate + malate or glycerol 3-phosphate conditions, but inhibited succinate-supported ROS accumulation. These results show that Zn2+ blocks mitochondrial function in all physiologically relevant substrate conditions. (C) 2004 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
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