Involvement of Oxidative Stress on the Impairment of Energy Metabolism Induced by Aβ Peptides on PC12 Cells: Protection by Antioxidants
Open accessAbstract
Alzheimer's disease is widely held to be associated with oxidative stress due, in part, to the membrane action of amyloid beta-peptide (A beta) aggregates. In this study, the involvement of oxidative stress on A beta-induced energy metabolism dysfunction was evaluated on PC12 cells. It was shown that A beta peptides (A beta25-35 and A beta1-40) induce a concentration-dependent accumulation of reactive oxygen species (ROS), decrease the cellular redox activity, and lead to the depletion of ATP levels. The observed inhibition by A beta of mitochondrial function and of glycolysis is blocked by the antioxidants vitamin E, idebenone, and GSH ethyl ester. Taken together, these data suggest that exposure of PC12 cells to A beta results in an impairment of energy metabolism, leading to a deficit in ATP levels and to the compromise of cellular viability. Furthermore, the generation of ROS seems to be a crucial event responsible for the energetic metabolic dysfunction induced by A beta.
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Idebenone protects neuronal cells against β-amyloid induced toxicity.
“Idebenone protects neuronal cells against β-amyloid induced toxicity164.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [164]
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- Authors
- Pereira, C., Santos, M. S., & Oliveira, C.
- Affiliations
- University of Coimbra (PT)
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 1999-06
- Volume
- 6
- Issue
- 3
- Pages
- 209-219
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2077113902
- Cited by
- 156
- References
- 65
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 1 · 2019: 2 · 2018: 2 · 2016: 6 · 2015: 2 · 2014: 6 · 2013: 4 · 2012: 2
- FWCI
- 5.66
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- amyloid-beta, oxidative stress, energy metabolism, PC12 cells, reactive oxygen species, ATP depletion, mitochondrial dysfunction, glycolysis, antioxidants, vitamin E, idebenone, glutathione ethyl ester, Alzheimer's disease, redox activity
- MeSH terms
- Adenosine Triphosphate, Animals, Antioxidants, Electron Transport Complex IV, Deoxyglucose, Dose-Response Relationship, Drug, Electron Transport, Glutathione, Glycolysis, Mitochondria, Multienzyme Complexes, Neurons, Oxidoreductases, Peptide Fragments, Succinate Dehydrogenase, Tritium, Electron Transport Complex III, Ubiquinone, Vitamin E, Benzoquinones, Amyloid beta-Peptides, NAD(P)H Dehydrogenase (Quinone), PC12 Cells, Oxidative Stress, Neuroprotective Agents, Pyruvic Acid, Electron Transport Complex II, Rats
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