The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Coenzyme Q10 and nicotinamide block striatal lesions produced by the mitochondrial toxin malonate
Abstract
A potential mechanism of neuronal injury in neurodegenerative diseases is a defect in energy metabolism that may lead to slow excitotoxic neuronal death. Consistent with this possibility, we showed that specific inhibitors of the electron transport chain produce excitotoxic lesions in vivo. In the present study we examined whether agents that improve energy metabolism can block lesions produced by the mitochondrial toxin malonate. Striatal lesions produced by the complex II inhibitor malonate were blocked in a dose‐dependent manner by oral pretreatment with coenzyme Q 10. Administration of nicotinamide by Alzet pump for 1 week attenuated malonate‐induced lesions, but riboflavin had no effect. Administration of nicotinamide intraperitoneally just prior to and following induction of the lesions produced dose‐dependent neuroprotection. A combination of coenzyme Q 10 with nicotinamide was more effective than either compound alone, as shown by both lesion size and magnetic resonance imaging in vivo. Both coenzyme Q 10 and nicotinamide blocked adenosine triphosphate depletions and lactate increases. These results confirm that mitochondrial toxins produce striatal excitotoxic lesions by a mechanism involving energy depletion in vivo. Furthermore, they suggest novel neuroprotective strategies that may be useful in the treatment of both mitochondrial encephalopathies and neurodegenerative diseases.
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In the citing paper
“Oral administration of CoQ10 exerts significant neuroprotective effects against striatal lesions in rats produced by aminoxyacetic acid, and the mitochondrial toxins malonate and 3-NP148-150.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [148]
In the citing paper
“Oral administration of CoQ10 produced dose-dependent neuroprotective effects against malonate induced striatal lesions, depletion of ATP and increases in lactate concentration148.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [148]
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Cites
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Fluorometric assay of proteins in the nanogram range
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Ubiquinol-10 is an effective lipid-soluble antioxidant at physiological concentrations.
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Alternative excitotoxic hypotheses
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Research works printed but not linked: 6
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Aging, energy, and oxidative stress in neurodegenerative diseases
Beal, M. F. (1995) · Annals of Neurology · doi:10.1002/ana.410380304 · Cited by 1,434
Self-citationGilgun‐Sherki, Y., Melamed, E., & Offen, D. (2001) · Neuropharmacology · doi:10.1016/s0028-3908(01)00019-3 · Cited by 850
Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism
Golomb, B. A., & Evans, M. A. (2008) · American Journal of Cardiovascular Drugs · doi:10.2165/0129784-200808060-00004 · Cited by 677
Matthews, R. T., Yang, L., Browne, S., Baik, M., & Beal, M. F. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.15.8892 · Cited by 557
Self-citationMitochondria, Oxidative Damage, and Inflammation in Parkinson's Disease
Beal, M. F. (2003) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2003.tb07470.x · Cited by 529
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Metadata
- Authors
- Beal, M. F., Henshaw, D. R., Jenkins, B. G., Rosen, B. R., & Schulz, J. B.
- Affiliations
- Massachusetts General Hospital (US)
- Harvard University (US)
- Corresponding author
- Beal, M. Flint
- ORCID
- Rosen, Bruce R.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1994-12
- Volume
- 36
- Issue
- 6
- Pages
- 882-888
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W1965876571
- Cited by
- 189
- References
- 35
- Citations by year
- 2026: 1 · 2024: 5 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 2 · 2017: 1 · 2016: 3 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 6
- FWCI
- 2.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p01ns031579-05)
- U.S. Public Health Service (16367)
- National Institute of Neurological Disorders and Stroke (NS10828, NS31579)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Keywords
- coenzyme Q10, nicotinamide, malonate, mitochondrial toxins, striatal lesions, excitotoxicity, neuroprotection, mitochondrial bioenergetics, electron transport inhibition, complex II inhibition, ATP depletion, lactate, mitochondrial encephalopathy, neurodegenerative diseases
- MeSH terms
- Animals, Coenzymes, Corpus Striatum, Dose-Response Relationship, Drug, Magnetic Resonance Imaging, Male, Malonates, Mitochondria, Niacinamide, Ubiquinone, Rats, Sprague-Dawley, Rats
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