Cited by 273Genomics, phytochemicals, and oxidative stressNuclear Receptors and SignalingParkinson's Disease Mechanisms and Treatments

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Induction of the Nrf2-driven Antioxidant Response Confers Neuroprotection during Mitochondrial Stress in Vivo

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Shih, Andy Y., Imbeault, Sophie, Barakauskas, Vilte, Erb, Heidi, Jiang, Lei, Li, Ping, Murphy, Timothy H.·2005·Journal of Biological Chemistry

DOI 10.1074/jbc.m414635200

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Abstract

NF-E2 related factor (Nrf2) controls a pleiotropic cellular defense, where multiple antioxidant/detoxification pathways are up-regulated in unison. Although small molecule inducers of Nrf2 activity have been reported to protect neurons in vitro, whether similar pathways can be accessed in vivo is not known. We have investigated whether in vivo toxicity of the mitochondrial complex II inhibitor 3-nitropropionic acid (3-NP) can be attenuated by constitutive and inducible Nrf2 activity. The absence of Nrf2 function in Nrf2(-/-) mice resulted in 3-NP hypersensitivity that became apparent with time and increasing dose, causing motor deficits and striatal lesions on a more rapid time scale than identically treated Nrf2(+/+) and Nrf2(+/-) controls. Striatal succinate dehydrogenase activity, the target of 3-NP, was inhibited to the same extent in all genotypes by a single acute dose of 3-NP, suggesting that brain concentrations of 3-NP were similar. Dietary supplementation with the Nrf2 inducer tert-butylhydroquinone attenuated 3-NP toxicity in Nrf2(+/-) mice, but not Nrf2(-/-), confirming the Nrf2-specific action of the inducer in vivo. Increased Nrf2 activity alone was sufficient to protect animals from 3-NP toxicity because intrastriatal adenovirus-mediated Nrf2 overexpression significantly reduced lesion size compared with green fluorescent protein overexpressing controls. In cultured astrocytes, 3-NP was found to increase Nrf2 activity leading to antioxidant response element-dependent gene expression providing a potential mechanism for the increased sensitivity of Nrf2(-/-) animals to 3-NP toxicity in vivo. We conclude that Nrf2 may underlie a feedback system limiting oxidative load during chronic metabolic stress.

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Authors: Shih, A. Y., Imbeault, S., Barakauskas, V., Erb, H., Jiang, L., Li, P., & Murphy, T. H.
Affiliations: University of British Columbia (CA)
Corresponding author: Murphy, Timothy H.
ORCID: Shih, Andy Y.
Imbeault, Sophie
Barakauskas, Vilte
Jiang, Lei
Li, Ping
Murphy, Timothy H.
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 2005-06
Volume: 280
Issue: 24
Pages: 22925-22936
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.m414635200
OpenAlex: W2028243150
Cited by: 273
References: 80
Citations by year: 2026: 7 · 2025: 4 · 2024: 9 · 2023: 3 · 2022: 4 · 2021: 10 · 2020: 8 · 2019: 7 · 2018: 17 · 2017: 11 · 2016: 16 · 2015: 13 · 2014: 12 · 2013: 17 · 2012: 26
FWCI: 5.61
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 5600 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: Heart and Stroke Foundation of Canada
University of Ottawa
Rick Hansen Institute
Canadian Stroke Network
Michael Smith Health Research BC
University of British Columbia
Canadian Institutes of Health Research
Natural Sciences and Engineering Research Council of Canada
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords: Nrf2, antioxidant response element, neuroprotection, mitochondrial complex II inhibition, 3-nitropropionic acid, succinate dehydrogenase, striatal lesions, motor impairment, tert-butylhydroquinone, Nrf2 inducers, oxidative stress, astrocytes, adenoviral overexpression, Nrf2 knockout mice, metabolic stress
MeSH terms: Adenoviridae, Alkaline Phosphatase, Animals, Antioxidants, Astrocytes, Behavior, Animal, Brain, DNA-Binding Proteins, Dose-Response Relationship, Drug, Female, Genotype, Glutathione, Hydroquinones, Immunohistochemistry, Male, Mice, Transgenic, Mitochondria, Neuroglia, Neurons, Nitro Compounds, Placenta, Plasmids, Propionates, Succinate Dehydrogenase, Time Factors, Transfection, Blotting, Western, Trans-Activators, Up-Regulation, Rats, Wistar, DNA Primers, Oxidative Stress, COS Cells, Dietary Supplements, Reverse Transcriptase Polymerase Chain Reaction, Green Fluorescent Proteins, NF-E2-Related Factor 2, Mice, Rats

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Induction of the Nrf2-driven Antioxidant Response Confers Neuroprotection during Mitochondrial Stress in Vivo

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