ReviewBioMed research international2013
Oxidative stress induces mitochondrial DNA damage and cytotoxicity through independent mechanisms in human cancer cells.
Review in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 80 citations in OpenAlex.
- A moderate increase in dietary zinc reduces DNA strand breaks in leukocytes and alters plasma proteins without changing plasma zinc concentrations.The American journal of clinical nutrition · 2017Trial
- Improved oxidative status in major abdominal surgery patients after N-acetyl cystein supplementation.Nutrition journal · 2015Trial
- Mitochondrial Dysfunctions in Human Primary Coenzyme QBiomolecules · 2026Review
- Impeding the NHEJ Pathway for Overcoming Radioresistance in the Context of Precision Radiotherapy of Cancer.Pharmaceutics · 2026Review
- Oxidative Stress Biomarkers in Laryngeal Squamous Cell Carcinoma and Their Clinical Implications: Preliminary Results.Biomedicines · 2025Article
- Resveratrol Reduces ROS by Increasing GSH in Vitrified Sheep Embryos.Animals : an open access journal from MDPI · 2023Article
- Melatonin Repairs Osteoporotic Bone Defects in Iron-Overloaded Rats through PI3K/AKT/GSK-3Oxidative medicine and cellular longevity · 2023Article
- Insights regarding mitochondrial DNA copy number alterations in human cancer (Review).International journal of molecular medicine · 2022Review
- Oxidation, Glycation, and Carbamylation of Salivary Biomolecules in Healthy Children, Adults, and the Elderly: Can Saliva Be Used in the Assessment of Aging?Journal of inflammation research · 2022Article
- Regulation of mitochondrial dysfunction induced cell apoptosis is a potential therapeutic strategy for herbal medicine to treat neurodegenerative diseases.Frontiers in pharmacology · 2022Review
- Bridging Cyanobacteria to Neurodegenerative Diseases: A New Potential Source of Bioactive Compounds against Alzheimer's Disease.Marine drugs · 2021Review
- Article
- Mitochondrial Stress Response and Cancer.Trends in cancer · 2020Review
- Mitochondrial Dysfunction and Inflammaging in Heart Failure: Novel Roles of CYP-Derived Epoxylipids.Cells · 2020Review
- Lung cancer increases HHeliyon · 2020Article
- The risks of ubiquinone and β-carotene deficiency and metabolic disorders in patients with oral cancer.BMC cancer · 2020Article
- Anti-neuroinflammation ameliorates systemic inflammation-induced mitochondrial DNA impairment in the nucleus of the solitary tract and cardiovascular reflex dysfunction.Journal of neuroinflammation · 2019Article
- Apple Peel Flavonoid Fraction 4 Suppresses Breast Cancer Cell Growth by Cytostatic and Cytotoxic Mechanisms.Molecules (Basel, Switzerland) · 2019Article
- Metabolic signatures suggest o-phosphocholine to UDP-N-acetylglucosamine ratio as a potential biomarker for high-glucose and/or palmitate exposure in pancreatic β-cells.Metabolomics : Official journal of the Metabolomic Society · 2019Article
- Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer's Disease.Frontiers in neuroscience · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrinsic oxidative stress through increased production of reactive oxygen species (ROS) is associated with carcinogenic transformation, cell toxicity, and DNA damage. Mitochondrial DNA (mtDNA) is a natural surrogate to oxidative DNA damage. MtDNA damage results in the loss of its supercoiled structure and is readily detectable using a novel, supercoiling-sensitive real-time PCR method. Our studies have demonstrated that mtDNA damage, as measured by DNA strand breaks and copy number depletion, is very sensitive to exogenous H2O2 but independent of endogenous ROS production in both prostate cancer and normal cells. In contrast, aggressive prostate cancer cells exhibit a more than 10-fold sensitivity to H2O2-induced cell toxicity than normal cells, and a cascade of secondary ROS production is a critical determinant to the differential response. We propose a new paradigm to account for different mechanisms governing cellular oxidative stress, cell toxicity, and DNA damage with important ramifications in devising new techniques and strategies in prostate cancer prevention and treatment.
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What OpenQuestion holds
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.