Cited by 292Redox biology and oxidative stressNeonatal and fetal brain pathologyAntioxidant Activity and Oxidative Stress

Glutathione peroxidase-catalase cooperativity is required for resistance to hydrogen peroxide by mature rat oligodendrocytes

Open access
Baud, Olivier, Greene, Amanda E., Li, Jianrong, Wang, Hong, Volpe, Joseph J., Rosenberg, Paul A.·2004·The Journal of Neuroscience

Abstract

Oxidative mechanisms of injury are important in many neurological disorders, including hypoxic-ischemic brain damage. Cerebral palsy after preterm birth is hypothesized to be caused by hypoxic-ischemic injury of developing oligodendrocytes (OLs). Here we examined the developmental sensitivity of OLs to exogenous hydrogen peroxide (H2O2) with stage-specific rat oligodendrocyte cultures. We found that H2O2 itself or that generated by glucose oxidase was more toxic to developing than to mature OLs. Mature OLs were able to degrade H2O2 faster than developing OLs, suggesting that higher antioxidant enzyme activity might be the basis for their resistance. Catalase expression and activity were relatively constant during oligodendrocyte maturation, whereas glutathione peroxidase (GPx) was upregulated with a twofold to threefold increase in its expression and activity. Thus, it appeared that the developmental change in resistance to H2O2 was caused by modulation of GPx but not by catalase expression. To test the relative roles of catalase and GPx in the setting of oxidative stress, we measured enzyme activity in cells exposed to H2O2 and found that H2O2 induced a decrease in catalase activity in developing but not in mature OLs. Inhibition of GPx by mercaptosuccinate led to an increase in the vulnerability of mature OLs to H2O2 as well as a reduction in catalase activity. Finally, H2O2-dependent inactivation of catalase in developing OLs was prevented by the GPx mimic ebselen. These data provide evidence for a key role for GPx-catalase cooperativity in the resistance of mature OLs to H2O2-induced cell death.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1523/jneurosci.3989-03.2004

Cites

46 of 46 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Baud, O., Greene, A. E., Li, J., Wang, H., Volpe, J. J., & Rosenberg, P. A.
Affiliations
Boston Children's Hospital (US)
Corresponding author
Rosenberg, Paul A.
Venue
The Journal of Neuroscience
Published
2004-02-18
Volume
24
Issue
7
Pages
1531-1540
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W2024367623
Cited by
292
References
46
Citations by year
2026: 4 · 2025: 17 · 2024: 7 · 2023: 12 · 2022: 10 · 2021: 14 · 2020: 14 · 2019: 13 · 2018: 16 · 2017: 17 · 2016: 13 · 2015: 12 · 2014: 15 · 2013: 14 · 2012: 12
FWCI
5.70
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (NS38475, P01NS038475)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD18655, P30HD018655)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
glutathione peroxidase, catalase, hydrogen peroxide, oligodendrocyte maturation, oxidative stress, antioxidant enzymes, catalase inactivation, ebselen, mercaptosuccinic acid, hypoxic-ischemic brain injury, cerebral palsy, oxidative cell death, developmental vulnerability
MeSH terms
Animals, Catalase, Cell Differentiation, Cells, Cultured, Drug Resistance, Glutathione Peroxidase, Hydrogen Peroxide, Oligodendroglia, Peroxides, Time Factors, Up-Regulation, Oxidants, Rats, Sprague-Dawley, Apoptosis, Oxidative Stress, In Situ Nick-End Labeling, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review