Zinc inhibition of cellular energy production: implications for mitochondria and neurodegeneration
Article first published online: 4 APR 2003
Journal of Neurochemistry
Volume 85, Issue 3, pages 563–570, May 2003
How to Cite
Dineley, K. E., Votyakova, T. V. and Reynolds, I. J. (2003), Zinc inhibition of cellular energy production: implications for mitochondria and neurodegeneration. Journal of Neurochemistry, 85: 563–570. doi: 10.1046/j.1471-4159.2003.01678.x
- Issue published online: 4 APR 2003
- Article first published online: 4 APR 2003
- Received August 29, 2002; accepted November 19, 2002.
- electron transport chain;
- permeability transition;
- reactive oxygen species;
- tricarboxylic acid cycle
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.