ArticleMutation research2012
Prdx1 deficiency in mice promotes tissue specific loss of heterozygosity mediated by deficiency in DNA repair and increased oxidative stress.
Article in Mutation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
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- Catalase inhibits tumor growth by alleviating oxidative stress and promoting the polarization of tumor-associated macrophage from M2 to M1 phenotype in non-small cell lung cancer.Biology direct · 2026Article
- Pgk1 activation restores endothelial metabolic homeostasis to alleviate vascular aging and atherosclerosis.Cardiovascular diabetology · 2025Article
- An Adverse Outcome Pathway Network for Chemically Induced Oxidative Stress Leading to (Non)genotoxic Carcinogenesis.Chemical research in toxicology · 2023Review
- From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration.Frontiers in pharmacology · 2023Review
- The role of ROS in tumour development and progression.Nature reviews. Cancer · 2022Review
- Beneficial and Detrimental Effects of Reactive Oxygen Species on Lifespan: A Comprehensive Review of Comparative and Experimental Studies.Frontiers in cell and developmental biology · 2021Review
- Piecing Together How Peroxiredoxins Maintain Genomic Stability.Antioxidants (Basel, Switzerland) · 2018Review
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- Histone acetyltransferase KAT8 is essential for mouse oocyte development by regulating reactive oxygen species levels.Development (Cambridge, England) · 2017Article
- The Role of Redox-Regulating Enzymes in Inoperable Breast Cancers Treated with Neoadjuvant Chemotherapy.Oxidative medicine and cellular longevity · 2017Article
- Redox Regulating Enzymes and Connected MicroRNA Regulators Have Prognostic Value in Classical Hodgkin Lymphomas.Oxidative medicine and cellular longevity · 2017Article
- Peroxiredoxin 1 interacts with and blocks the redox factor APE1 from activating interleukin-8 expression.Scientific reports · 2016Article
- Total peroxiredoxin expression is associated with survival in patients with follicular lymphoma.Virchows Archiv : an international journal of pathology · 2016Article
- Comparison of skeletal muscle miRNA and mRNA profiles among three pig breeds.Molecular genetics and genomics : MGG · 2016Article
- Adenanthin, a new inhibitor of thiol-dependent antioxidant enzymes, impairs the effector functions of human natural killer cells.Immunology · 2015Article
- Oxidative stress preferentially induces a subtype of micronuclei and mediates the genomic instability caused by p53 dysfunction.Mutation research · 2014Article
- Nitrosative stress induces peroxiredoxin 1 ubiquitination during ischemic insult via E6AP activation in endothelial cells both in vitro and in vivo.Antioxidants & redox signaling · 2014Article
- Regulation of PRDX1 peroxidase activity by Pin1.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The loss of the H(2)O(2) scavenger protein encoded by Prdx1 in mice leads to an elevation of reactive oxygen species (ROS) and tumorigenesis of different tissues. Loss of heterozygosity (LOH) mutations could initiate tumorigenesis through loss of tumor suppressor gene function in heterozygous somatic cells. A connection between the severity of ROS and the frequency of LOH mutations in vivo has not been established. Therefore, in this study, we characterized in vivo LOH in ear fibroblasts and splenic T cells of 3-4 month old Prdx1 deficient mice. We found that the loss of Prdx1 significantly elevates ROS amounts in T cells and fibroblasts. The basal amounts of ROS were higher in fibroblasts than in T cells, probably due to a less robust Prdx1 peroxidase activity in the former. Using Aprt as a LOH reporter, we observed an elevation in LOH mutation frequency in fibroblasts, but not in T cells, of Prdx1(-/-) mice compared to Prdx1(+/+) mice. The majority of the LOH mutations in both cell types were derived from mitotic recombination (MR) events. Interestingly, Mlh1, which is known to suppress MR between divergent sequences, was found to be significantly down-regulated in fibroblasts of Prdx1(-/-) mice. Therefore, the combination of elevated ROS amounts and down-regulation of Mlh1 may have contributed to the elevation of MR in fibroblasts of Prdx1(-/-) mice. We conclude that each tissue may have a distinct mechanism through which Prdx1 deficiency promotes tumorigenesis.
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