Dissemin is shutting down on January 1st, 2025

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Wiley, Journal of Neurochemistry, 3(85), p. 563-570, 2003

DOI: 10.1046/j.1471-4159.2003.01678.x

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Zinc inhibition of cellular energy production: implications for mitochondria and neurodegeneration

Journal article published in 2003 by Kirk E. Dineley, Tatyana V. Votyakova, Ian J. Reynolds ORCID
This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

An increasing body of evidence suggests that high intracellular free zinc promotes neuronal death by inhibiting cellular energy production. A number of targets have been postulated, including complexes of the mitochondrial electron transport chain, components of the tricarboxylic acid cycle, and enzymes of glycolysis. Consequences of cellular zinc overload may include increased cellular reactive oxygen species (ROS) production, loss of mitochondrial membrane potential, and reduced cellular ATP levels. Additionally, zinc toxicity might involve zinc uptake by mitochondria and zinc induction of mitochondrial permeability transition. The present review discusses these processes with special emphasis on their potential involvement in brain injury.