The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Dysfunction of mitochondrial complex I and the proteasome: interactions between two biochemical deficits in a cellular model of Parkinson's disease
Abstract
Two biochemical deficits have been described in the substantia nigra in Parkinson's disease, decreased activity of mitochondrial complex I and reduced proteasomal activity. We analysed interactions between these deficits in primary mesencephalic cultures. Proteasome inhibitors (epoxomicin, MG132) exacerbated the toxicity of complex I inhibitors [rotenone, 1‐methyl‐4‐phenylpyridinium (MPP+)] and of the toxic dopamine analogue 6‐hydroxydopamine, but not of inhibitors of mitochondrial complex II–V or excitotoxins [N‐methyl‐d‐aspartate (NMDA), kainate]. Rotenone and MPP+ increased free radicals and reduced proteasomal activity via adenosine triphosphate (ATP) depletion. 6‐hydroxydopamine also increased free radicals, but did not affect ATP levels and increased proteasomal activity, presumably in response to oxidative damage. Proteasome inhibition potentiated the toxicity of rotenone, MPP+ and 6‐hydroxydopamine at concentrations at which they increased free radical levels ≥ 40% above baseline, exceeding the cellular capacity to detoxify oxidized proteins reduced by proteasome inhibition, and also exacerbated ATP depletion caused by complex I inhibition. Consistently, both free radical scavenging and stimulation of ATP production by glucose supplementation protected against the synergistic toxicity. In summary, proteasome inhibition increases neuronal vulnerability to normally subtoxic levels of free radicals and amplifies energy depletion following complex I inhibition.
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Cites
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Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
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Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
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“Mutations in the gene encoding parkin, an E3-ubiquitinligase (Shimura et al. 2000), led to autosomal recessive juvenile parkinsonism (Kitada et al.”
BackgroundMITOCHONDRIAL COMPLEX I DEFICIENCY IN PARKINSON'S DISEASE
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The ubiquitin pathway in Parkinson's disease
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Cited by
Mitochondria take center stage in aging and neurodegeneration
Beal, M. F. (2005) · Annals of Neurology · doi:10.1002/ana.20624 · Cited by 957
Mitochondria in the aetiology and pathogenesis of Parkinson's disease
Schapira, A. H. (2008) · The Lancet Neurology · doi:10.1016/s1474-4422(07)70327-7 · Cited by 883
Expanding insights of mitochondrial dysfunction in Parkinson's disease
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Barja, G. (2004) · Trends in Neurosciences · doi:10.1016/j.tins.2004.07.005 · Cited by 653
Alexander, G. E. (2004) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2004.6.3/galexander · Cited by 523
Metadata
- Authors
- Höglinger, G. U., Carrard, G., Michel, P. P., Medja, F., Lombès, A., Ruberg, M., Friguet, B., & Hirsch, E. C.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2003-08-11
- Volume
- 86
- Issue
- 5
- Pages
- 1297-1307
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1503570667
- Cited by
- 253
- References
- 48
- FWCI
- 14.29
- Type
- journal article
- Language
- en
- Open access
- closed
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- Höglinger, G. U., Carrard, G., Michel, P. P., Medja, F., Lombès, A., Ruberg, M., Friguet, B., & Hirsch, E. C. (2003). Dysfunction of mitochondrial complex I and the proteasome: interactions between two biochemical deficits in a cellular model of Parkinson's disease. Journal of Neurochemistry. https://doi.org/10.1046/j.1471-4159.2003.01952.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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