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Cited by 89Redox biology and oxidative stressImmunotoxicology and immune responsesNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 67 of the 69 references it cites were found in a registry or an index.

Methamphetamine-Induced TNF-α Gene Expression and Activation of AP-1 in Discrete Regions of Mouse Brain

Toborek, Michal, Flora, Govinder, Lee, Yong Woo, Nath, Avindra, Maragos, William, Hennig, Bernhard·2002·NeuroMolecular Medicine
DOI 10.1385/nmm:2:1:71
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Abstract

Cellular and molecular mechanisms of methamphetamine (METH)-induced neurotoxicity may involve alterations of cellular redox status and induction of inflammatory genes. To study this hypothesis, molecular signaling pathways of METH-induced inflammatory responses via activation of redox-sensitive transcription factors were investigated in discrete regions (corpus striatum, frontal cortex, and hippocampus) of mouse brain. Intraperitoneal injection of METH at a dose of 10 mg/kg body weight resulted in a significant increase in oxidative stress, as measured by 2,7-dichlorofluorescein (DCF) fluorescence assay, thiobarbituric acid-reactive substances (TBARS), and total glutathione levels. Glutathione peroxidase activity was also significantly increased after METH exposure. In addition, DNA binding activity of activator protein-1 (AP-1), a redox-responsive transcription factor, was increased in all studied brain regions in response to METH treatment. Because AP-1 is known to regulate expression of inflammatory genes, levels of TNF-alpha mRNA were also studied. Expression of the tumor necrosis factor-alpha (TNF-alpha) gene was induced 3 h after METH injection and remained elevated for up to 6 h of METH exposure. In addition, stimulation of the TNF-alpha gene was associated with increased TNF-a protein production in the frontal cortex. These results suggest that METH-induced disturbances in cellular redox status and that activation of AP-1 can play a critical role in signaling pathways leading to upregulation of inflammatory genes in vivo. Furthermore, these data provide evidence for the role of oxidative stress in the neurotoxic effects of METH.

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Metadata

Authors
Toborek, M., Flora, G., Lee, Y. W., Nath, A., Maragos, W., & Hennig, B.
Affiliations
University of Kentucky (US)
Corresponding author
Toborek, Michal
ORCID
Venue
NeuroMolecular Medicine
Publisher
Springer Science and Business Media LLC
Published
2002
Volume
2
Issue
1
Pages
71-85
ISSN
1535-1084 (ISSN-L)
DOI
10.1385/nmm:2:1:71
OpenAlex
W1542501108
Cited by
89
References
69
Citations by year
2026: 1 · 2025: 4 · 2023: 4 · 2022: 4 · 2021: 2 · 2020: 5 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 8 · 2014: 8 · 2013: 1 · 2012: 6
FWCI
0.93
Type
journal article
Language
en
Open access
closed
Locations
  • NeuroMolecular Medicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (MH 63022, R01MH063022)
  • National Institute of Neurological Disorders and Stroke (R01NS039254, NS-39254)
  • National Institute of Environmental Health Sciences (P42ES007380)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
methamphetamine, neurotoxicity, TNF-alpha gene expression, activator protein-1, oxidative stress, redox-sensitive transcription factors, inflammatory gene expression, glutathione peroxidase, striatum, frontal cortex, hippocampus, brain regions
MeSH terms
Central Nervous System Stimulants, Animals, Brain Chemistry, Corpus Striatum, DNA, Frontal Lobe, Glutathione, Glutathione Peroxidase, Hippocampus, Inflammation, Injections, Intraperitoneal, Male, Methamphetamine, Mice, Inbred C57BL, Nerve Tissue Proteins, Transcription, Genetic, Tumor Necrosis Factor-alpha, Lipid Peroxidation, Dopamine Agents, Signal Transduction, Thiobarbituric Acid Reactive Substances, Oxidative Stress, Transcription Factor AP-1, Mice

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