Cited by 156Alzheimer's disease research and treatmentsMitochondrial Function and PathologyRedox biology and oxidative stress

Involvement of Oxidative Stress on the Impairment of Energy Metabolism Induced by Aβ Peptides on PC12 Cells: Protection by Antioxidants

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Pereira, Cláudia, Santos, Maria Sancha, Oliveira, Catarina·1999·Neurobiology of Disease

Abstract

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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Crossref · 10.1006/nbdi.1999.0241

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64 of 64 references verified0 citation errors · 0 not checkable

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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
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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