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Zinc inhibition of cellular energy production: implications for mitochondria and neurodegeneration
Author(s) -
Dineley Kirk E.,
Votyakova Tatyana V.,
Reynolds Ian J.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2003.01678.x
Subject(s) - mitochondrion , neurodegeneration , citric acid cycle , microbiology and biotechnology , zinc , glycolysis , mitochondrial permeability transition pore , reactive oxygen species , intracellular , biology , biochemistry , membrane permeability , tricarboxylic acid , chemistry , programmed cell death , enzyme , apoptosis , membrane , medicine , disease , organic chemistry
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.