ReviewMutation research
Role of oxidatively induced DNA lesions in human pathogenesis.
Review in Mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 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
147 citing papers in PubMed, 328 citations in OpenAlex.
- The 2024 Lebanon conflict: a multidimensional assessment of syndemic impacts on public health and sustainable development goals.Internal and emergency medicine · 2026Review
- DNA Structure-Dependent Enrichment of Oxidative Lesions.Chemical research in toxicology · 2026Article
- Probiotic intervention mitigates radiation-induced intestinal injury by alleviating oxidative stress in a human gut-on-a-chip.Scientific reports · 2026Article
- Nanoencapsulation of Anise oil and evaluation of its antimicrobial and antioxidant effects to propose for food preservation.Discover nano · 2026Article
- The Bright and Dark Sides of Nitric Oxide in Neurodegenerative Diseases.Journal of personalized medicine · 2026Review
- Nutritional Strategies and Aging: Current Evidence and Future Directions.Molecules (Basel, Switzerland) · 2026Review
- Phytochemicals and REDOX Modulation: Molecular Mechanisms, Clinical Relevance, and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Microbiome-driven resistance in cervical cancer therapy: from mechanistic dissection to clinical translation.Expert reviews in molecular medicine · 2025Review
- Molecular mechanisms of air pollution-induced carcinogenesis and the emerging role of microplastics.Human genomics · 2025Review
- Nitro-oxidative nucleotide modifications in plants and associated microorganisms: signalling sensors or stress symptoms?Journal of experimental botany · 2025Review
- The Role of Oxidative Stress in the Relationship Between Periodontitis and Alzheimer's Disease: A Review of the Literature.Journal of personalized medicine · 2025Review
- Five glutathione S-transferase isozymes played crucial role in the detoxification of aflatoxin BJournal of animal science and biotechnology · 2025Article
- Article
- What tunes guanine ionization potential in a nucleosome? An all-in-one systematic QM/MM assessment.Biophysical journal · 2024Article
- Review
- Early oxidative stress and DNA damage in Aβ-burdened hippocampal neurons in an Alzheimer's-like transgenic rat model.Communications biology · 2024Article
- Assessing the antioxidant properties of Naringin and Rutin and investigating their oxidative DNA damage effects in breast cancer.Scientific reports · 2024Article
- Article
- Tumor-resident Lactobacillus iners confer chemoradiation resistance through lactate-induced metabolic rewiring.Cancer cell · 2023Article
- Differential Modulation of Markers of Oxidative Stress and DNA Damage in Arterial Hypertension.Antioxidants (Basel, Switzerland) · 2023Article
87 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Genome stability is essential for maintaining cellular and organismal homeostasis, but it is subject to many threats. One ubiquitous threat is from a class of compounds known as reactive oxygen species (ROS), which can indiscriminately react with many cellular biomolecules including proteins, lipids, and DNA to produce a variety of oxidative lesions. These DNA oxidation products are a direct risk to genome stability, and of particular importance are oxidative clustered DNA lesions (OCDLs), defined as two or more oxidative lesions present within 10 bp of each other. ROS can be produced by exposure of cells to exogenous environmental agents including ionizing radiation, light, chemicals, and metals. In addition, they are produced by cellular metabolism including mitochondrial ATP generation. However, ROS also serve a variety of critical cellular functions and optimal ROS levels are maintained by multiple cellular antioxidant defenses. Oxidative DNA lesions can be efficiently repaired by base excision repair or nucleotide excision repair. If ROS levels increase beyond the capacity of its antioxidant defenses, the cell's DNA repair capacity can become overwhelmed, leading to the accumulation of oxidative DNA damage products including OCDLs, which are more difficult to repair than individual isolated DNA damage products. Here we focus on the induction and repair of OCDLs and other oxidatively induced DNA lesions. If unrepaired, these lesions can lead to the formation of mutations, DNA DSBs, and chromosome abnormalities. We discuss the roles of these lesions in human pathologies including aging and cancer, and in bystander effects.
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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.