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

Journal of Neurochemistry - Tập 85 Số 3 - Trang 563-570 - 2003
Kirk E. Dineley1, Tatyana V. Votyakova2, Ian J. Reynolds2
1Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261 USA
2Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

Tóm tắt

AbstractAn 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.

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Tài liệu tham khảo

10.1046/j.1471-4159.2000.0751878.x

10.1073/pnas.95.1.358

10.1006/exnr.2000.7438

10.1016/S0005-2728(00)00182-1

Brierley G. P., 1967, Ion transport by heart mitochondria. VII. Activation of the energy‐linked accumulation of Mg++ by Zn++ and other cations, J. Biol. Chem., 242, 1115

10.1021/bi00864a035

10.1016/0003-9861(68)90584-5

10.1074/jbc.275.18.13441

Canzoniero L. M. T., 1999, Measurement of intracellular free zinc concentrations accompanying zinc‐ induced neuronal death, J. Neurosci., 19, 1

10.1016/0003-9861(68)90051-9

10.1046/j.1471-4159.1998.71062401.x

10.1146/annurev.neuro.21.1.347

10.1016/S0006-8993(98)00463-6

10.1006/nbdi.2000.0303

Dineley K. E., 2001, Zn2+ causes loss of membrane and alters production of reactive oxygen species in isolated brain mitochondria, Soc. Neurosci. Abstract., 27, 2311

10.1124/mol.62.3.618

10.1016/S0074-7742(08)60279-2

10.1046/j.1471-4159.1999.0722488.x

10.1074/jbc.M108264200

10.1016/S0021-9258(19)83641-4

10.1016/S0021-9258(19)52312-2

10.1016/0006-3002(56)90282-7

10.3177/jnsv.26.357

10.1073/pnas.95.16.9146

10.1074/jbc.M108834200

10.1074/jbc.M200910200

Kelly E. J., 1996, Metallothionein I and II protect against zinc deficiency and zinc toxicity in mice, J. Nutr., 126, 1782

Kenakin T., 1993, Pharmacologic Analysis of Drug–Receptor Interaction, 385

10.1046/j.1460-9568.1999.00437.x

10.1016/S0006-8993(00)02944-9

10.1016/0003-9861(74)90148-9

10.1016/0014-5793(72)80802-0

10.1126/science.272.5264.1013

10.1016/0020-711X(92)90078-F

Lee J. Y., 2000, Accumulation of zinc in degenerating hippocampal neurons of ZnT3‐null mice after seizures: evidence against synaptic vesicle origin, J. Neurosci. (Online), 20, RC79, 10.1523/JNEUROSCI.20-11-j0003.2000

10.1074/jbc.270.42.25001

10.1111/j.1432-1033.1991.tb15944.x

10.1016/S0009-2797(00)00243-X

10.1093/jn/128.4.667

Nelson D. L., 2000, Lehninger Principles of Biochemistry, 1152

10.1021/bi00841a038

10.1523/JNEUROSCI.20-23-j0001.2000

10.1046/j.1471-4159.1999.721609.x

10.1126/science.1060331

10.1006/taap.1995.1216

10.1073/pnas.95.15.8428

10.1002/j.1460-2075.1995.tb07042.x

10.1016/0014-5793(94)01256-3

10.1523/JNEUROSCI.17-24-09554.1997

10.1073/pnas.96.5.2414

10.1523/JNEUROSCI.20-09-03139.2000

10.1016/0006-291X(67)90242-2

Tsien R. Y., 1999, Calcium as a Cellular Regulator, 28

Tsuda M., 1997, Expression of zinc transporter gene, ZnT‐1, is induced after transient forebrain ischemia in the gerbil, J. Neurosci., 17, 6678, 10.1523/JNEUROSCI.17-17-06678.1997

10.1016/0896-6273(93)90240-R

10.1016/S0165-6147(00)01541-8

10.1006/abbi.1998.1058

10.1073/pnas.041619198

10.1038/35048073

10.1074/jbc.275.11.7534

10.1016/0304-4157(95)00003-A