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Cited by 101Redox biology and oxidative stressGenetics, Aging, and Longevity in Model OrganismsAntioxidant Activity and Oxidative Stress

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.

Progeric effects of catalase inactivation in human cells

Koepke, Jay I., Wood, Christopher S., Terlecky, Laura J., Walton, Paul A., Terlecky, Stanley R.·2008·Toxicology and Applied Pharmacology
DOI 10.1016/j.taap.2008.06.004
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Abstract

Peroxisomes generate hydrogen peroxide, a reactive oxygen species, as part of their normal metabolism. A number of pathological situations exist in which the organelle's capacity to degrade the potentially toxic oxidant is compromised. It is the peroxidase, catalase, which largely determines the functional antioxidant capacity of the organelle, and it is this enzyme that is affected in aging, in certain diseases, and in response to exposure to specific chemical agents. To more tightly control the enzymatic activity of peroxisomal catalase and carefully document the effects of its impaired action on human cells, we employed the inhibitor 3-amino-1,2,4-triazole. We show that by chronically reducing catalase activity to approximately 38% of normal, cells respond in a dramatic manner, displaying a cascade of accelerated aging reactions. Hydrogen peroxide and related reactive oxygen species are produced, protein and DNA are oxidatively damaged, import into peroxisomes and organelle biogenesis is corrupted, and matrix metalloproteinases are hyper-secreted from cells. In addition, mitochondria are functionally impaired, losing their ability to maintain a membrane potential and synthesize reactive oxygen species themselves. These latter results suggest an important redox-regulated connection between the two organelle systems, a topic of considerable interest for future study.

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Crossref · 10.1016/j.taap.2008.06.004

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  • CAT inactivation may lead, due to an impaired mitochondria-peroxisome cross-talk, to a condition of premature aging, also known as progeria phenotype.

    “CAT inactivation may lead, due to an impaired mitochondria-peroxisome cross-talk, to a condition of premature aging, also known as progeria phenotype [53].”

    From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [53]

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Metadata

Authors
Koepke, J. I., Wood, C. S., Terlecky, L. J., Walton, P. A., & Terlecky, S. R.
Affiliations
  • Wayne State University (US)
  • Western University (CA)
Corresponding author
Terlecky, Stanley R.
ORCID
Venue
Toxicology and Applied Pharmacology
Publisher
Elsevier BV
Published
2008-10
Volume
232
Issue
1
Pages
99-108
ISSN
0041-008X (ISSN-L)
DOI
10.1016/j.taap.2008.06.004
OpenAlex
W2012540688
Cited by
101
References
49
Citations by year
2026: 4 · 2025: 15 · 2023: 3 · 2022: 6 · 2021: 2 · 2020: 4 · 2019: 3 · 2018: 4 · 2017: 7 · 2016: 4 · 2015: 5 · 2014: 3 · 2013: 12 · 2012: 11
FWCI
2.47
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Toxicology and Applied Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p30es006639-15)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK056299, DK-56299)
  • National Institute of Environmental Health Sciences (1 P30 ES06639)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Keywords
catalase inactivation, peroxisomes, 3-amino-1,2,4-triazole, hydrogen peroxide, reactive oxygen species, oxidative DNA damage, protein oxidation, peroxisome biogenesis, matrix metalloproteinases, mitochondrial dysfunction, mitochondrial membrane potential, mitochondrial reactive oxygen species, aging, peroxisomal dysfunction, redox regulation
MeSH terms
Peroxisome-Targeting Signal 1 Receptor, Amitrole, Catalase, Cell Line, DNA Damage, Dose-Response Relationship, Drug, Enzyme Activation, Enzyme Inhibitors, Fibroblasts, Humans, Hydrogen Peroxide, Mitochondria, Oxidation-Reduction, Time Factors, Cellular Senescence, Reactive Oxygen Species, Receptors, Cytoplasmic and Nuclear, Oxidative Stress, Peroxisomes, Matrix Metalloproteinase 2, Cell Proliferation, Membrane Potential, Mitochondrial

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