ArticleOxidative medicine and cellular longevity2015
Intracellular oxidant activity, antioxidant enzyme defense system, and cell senescence in fibroblasts with trisomy 21.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Meta-analysis of metabolites involved in bioenergetic pathways reveals a pseudohypoxic state in Down syndrome.Molecular medicine (Cambridge, Mass.) · 2020Pooled it
- A Short-Term Resistance Training Circuit Improved Antioxidants in Sedentary Adults with Down Syndrome.Oxidative medicine and cellular longevity · 2021Trial
- Are Bioimpedance Parameters Altered in Adults With Down Syndrome? A Cross-Sectional Study.Journal of intellectual disability research : JIDR · 2026Article
- Elevated Senescence Markers in Developing Trisomy 21 Human Lungs.American journal of respiratory cell and molecular biology · 2025Article
- Oxidative Stress and Down Syndrome: A Systematic Review.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?Aging and disease · 2025Review
- Implications of ALS-Associated Mutations on Biochemical and Biophysical Features of hSOD1 and Aggregation Formation.Biochemical genetics · 2024Article
- Chemical composition and toxicity studies onRSC advances · 2024Article
- Antioxidant Metabolism Pathways in Vitamins, Polyphenols, and Selenium: Parallels and Divergences.International journal of molecular sciences · 2024Review
- Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton reaction.Cell death & disease · 2022Article
- Biochemical Discrimination of the Down Syndrome-Related Metabolic and Oxidative/Nitrosative Stress Alterations from the Physiologic Age-Related Changes through the Targeted Metabolomic Analysis of Serum.Antioxidants (Basel, Switzerland) · 2022Article
- Human Trisomic iPSCs from Down Syndrome Fibroblasts Manifest Mitochondrial Alterations Early during Neuronal Differentiation.Biology · 2021Article
- Article
- Influence of Maternal Age and Gestational Age on Breast Milk Antioxidants During the First Month of Lactation.Nutrients · 2020Article
- Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials.Antioxidants (Basel, Switzerland) · 2020Review
- Therapeutic importance of hydrogen sulfide in age-associated neurodegenerative diseases.Neural regeneration research · 2020Review
- Challenges and Opportunities for Translation of Therapies to Improve Cognition in Down Syndrome.Trends in molecular medicine · 2020Article
- Cellular Senescence in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2020Review
- Accelerated bio-cognitive aging in Down syndrome: State of the art and possible deceleration strategies.Aging cell · 2019Review
- Elimination of protein aggregates prevents premature senescence in human trisomy 21 fibroblasts.PloS one · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down's syndrome (DS) is characterized by a complex phenotype associated with chronic oxidative stress and mitochondrial dysfunction. Overexpression of genes on chromosome-21 is thought to underlie the pathogenesis of the major phenotypic features of DS, such as premature aging. Using cultured fibroblasts with trisomy 21 (T21F), this study aimed to ascertain whether an imbalance exists in activities, mRNA, and protein expression of the antioxidant enzymes SOD1, SOD2, glutathione-peroxidase, and catalase during the cell replication process in vitro. T21F had high SOD1 expression and activity which led to an interenzymatic imbalance in the antioxidant defense system, accentuated with replicative senescence. Intracellular ROS production and oxidized protein levels were significantly higher in T21F compared with control cells; furthermore, a significant decline in intracellular ATP content was detected in T21F. Cell senescence was found to appear prematurely in DS cells as shown by SA-β-Gal assay and p21 assessment, though not apoptosis, as neither p53 nor the proapoptotic proteins cytochrome c and caspase 9 were altered in T21F. These novel findings would point to a deleterious role of oxidatively modified molecules in early cell senescence of T21F, thereby linking replicative and stress-induced senescence in cultured cells to premature aging in DS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.