Peroxisomes and oxidative stress
Open accessAbstract
The discovery of the colocalization of catalase with H2O2-generating oxidases in peroxisomes was the first indication of their involvement in the metabolism of oxygen metabolites. In past decades it has been revealed that peroxisomes participate not only in the generation of reactive oxygen species (ROS) with grave consequences for cell fate such as malignant degeneration but also in cell rescue from the damaging effects of such radicals. In this review the role of peroxisomes in a variety of physiological and pathological processes involving ROS mainly in animal cells is presented. At the outset the enzymes generating and scavenging H2O2 and other oxygen metabolites are reviewed. The exposure of cultured cells to UV light and different oxidizing agents induces peroxisome proliferation with formation of tubular peroxisomes and apparent upregulation of PEX genes. Significant reduction of peroxisomal volume density and several of their enzymes is observed in inflammatory processes such as infections, ischemia-reperfusion injury and hepatic allograft rejection. The latter response is related to the suppressive effects of TNFalpha on peroxisomal function and on PPARalpha. Their massive proliferation induced by a variety of xenobiotics and the subsequent tumor formation in rodents is evidently due to an imbalance in the formation and scavenging of ROS, and is mediated by PPARalpha. In PEX5-/- mice with the absence of functional peroxisomes severe abnormalities of mitochondria in different organs are observed which resemble closely those in respiratory chain disorders associated with oxidative stress. Interestingly, no evidence of oxidative damage to proteins or lipids, nor of increased peroxide production has been found in that mouse model. In this respect the role of PPARalpha, which is highly activated in those mice, in prevention of oxidative stress deserves further investigation.
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Peroxisomes proliferate or decrease in number in response to environmental stimuli, while impaired membrane growth related to ACBD5-deficiency may affect this dynamic process and reduce the responsiveness of the peroxisomal system to physiologic stressors.
“Peroxisomes proliferate or decrease in number in response to environmental stimuli, while impaired membrane growth related to ACBD5-deficiency may affect this dynamic process and reduce the responsiveness of the peroxisomal system to physiologic stressors (Darwisch et al., 2020;Schrader et al., 2006).”
From <scp>ACBD5</scp>‐related retinal dystrophy with leukodystrophy due to novel mutations in <i>ACBD5</i> and with additional features including ovarian insufficiency (2024) · cites this paper as Schrader et al., 2006
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BackgroundFission and proliferation of peroxisomes
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“…proliferate or decrease in number in response to environmental stimuli, while impaired membrane growth related to ACBD5-deficiency may affect this dynamic process and reduce the responsiveness of the peroxisomal system to physiologic stressors (Darwisch et al., 2020; Schrader et al., 2006).”
Background
- Authors
- Schrader, M., & Fahimi, H. D.
- Affiliations
- Philipps University of Marburg (DE)
- Corresponding author
- Schrader, Michael
- ORCID
- Schrader, Michael
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 1763
- Issue
- 12
- Pages
- 1755-1766
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W2049230829
- Cited by
- 838
- References
- 9
- Citations by year
- 2026: 43 · 2025: 46 · 2024: 36 · 2023: 54 · 2022: 58 · 2021: 62 · 2020: 50 · 2019: 43 · 2018: 45 · 2017: 50 · 2016: 37 · 2015: 41 · 2014: 39 · 2013: 35 · 2012: 33
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- peroxisomes, oxidative stress, reactive oxygen species, hydrogen peroxide, catalase, PEX genes, peroxisome proliferation, PPARα, TNF-α, mitochondrial abnormalities, respiratory chain disorders, ischemia-reperfusion injury
- MeSH terms
- Peroxisome-Targeting Signal 1 Receptor, Animals, Catalase, Hydrogen Peroxide, Mitochondria, Reactive Oxygen Species, Receptors, Cytoplasmic and Nuclear, Mice, Knockout, Oxidative Stress, Peroxisomes, PPAR alpha, Mice
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