ReviewArchives of toxicology2026
Pathophysiology of reactive oxygen species (ROS).
Review in Archives of toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- The Gut Microbiome as a Mechanistic Link Between the Planetary Health Diet and Healthy Aging.Nutrients · 2026Review
- Morin attenuates vancomycin-induced nephrotoxicity via Nrf-2/HO-1, SIRT1/PGC1α and AKT/FOXO1A pathways.Molecular biology reports · 2026Article
- Integrative RNA-Seq Analysis Reveals Stress Type-Dependent lncRNA-Centered Co-Expression Networks Across Human Cellular Stress Contexts.International journal of molecular sciences · 2026Article
- Contribution of One-Electron Oxidation of Purine and Pyrimidine Bases to the Photo- and Radiation-Induced Damage to Cellular DNA.Chemphyschem : a European journal of chemical physics and physical chemistry · 2026Review
- Process Optimization ofFoods (Basel, Switzerland) · 2026Article
- ROS-CaArchives of microbiology · 2026Article
- ML-171 Attenuates Pentylenetetrazole-Associated Oxidative and Apoptotic Injury Without Robust Suppression of Seizure Expression: An In Vitro and In Vivo Study.International journal of molecular sciences · 2026Article
- The Role of PGC-1α in Neurodegenerative Diseases: Molecular Mechanisms, Translational Challenges, and Therapeutic Potential.Molecular neurobiology · 2026Review
- Reactive oxygen species in plants: spatiotemporal organization, redox signaling, and stress adaptation.Planta · 2026Review
- Injectable bioactive hydrogels as pharmacological drug delivery platforms for post-myocardial infarction cardiac repair: therapeutic cargo engineering, stimuli-responsive release mechanisms, and translational perspectives.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Review
- Barbados aloe as a water-administered therapeutic against Pseudomonas aeruginosa infection in Clarias gariepinus: Effects on hemato-biochemical profiles, electrolyte homeostasis, antioxidant capacity, and tissue histology.Veterinary research communications · 2026Article
- Article
- Green-ExtractedAntioxidants (Basel, Switzerland) · 2026Article
- Endoplasmic Reticulum-Targeting NIR Cyanine ER800 Nanoparticles Promote Pyroptosis in Triple-Negative Breast Cancer.ACS applied materials & interfaces · 2026Article
- Dietary Antioxidants and Redox Signaling in Cancer Prevention: Mechanistic Insights and Metabolic Inflammation.Nutrients · 2026Review
- In vivo dynamic nuclear polarization magnetic resonance imaging reveals cardiac mitochondrial redox imbalance as an early indicator of heart failure.Redox biology · 2026Article
- Regulation by Ascorbic Acid and HOO• Radicals of Extracellular DNA Network Formation and Internalization Activity of Mononuclear Cells.Sovremennye tekhnologii v meditsine · 2026Article
- Reactive oxygen species (ROS) in cancer: from redox signaling and metabolic plasticity to therapeutic vulnerabilities.Exploration of targeted anti-tumor therapy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) are context-dependent mediators that function as second messengers at low, localized flux and as drivers of damage when production overruns buffering capacity. Outcomes are dictated by source identity, subcellular compartment and pulse kinetics—the “where–when–how much” rule. We synthesize advances (2015–2025) across principal generators—mitochondrial electron transport, NADPH oxidases, xanthine oxidoreductase and ER/peroxisomal oxidoreductases—to show how compartmental H2O2 microgradients encode reversible cysteine signaling, while iron-rich niches pivot chemistry toward peroxynitrite, Fenton-derived ·OH, lipid peroxidation and regulated cell death (apoptosis, ferroptosis, parthanatos). We integrate these mechanisms with endothelial dysfunction, innate immune priming, ECM remodeling and barrier failure across cardiovascular, metabolic, neurodegenerative, oncologic, pulmonary, renal and critical-illness contexts, emphasizing crosstalk with RNS/RSS and iron metabolism as key modulators. Methodologically, we advocate species-resolved, compartment-aware assessment—e.g., DHE → 2-OH-E⁺ HPLC for O2·−, targeted HyPer/roGFP-Orp for H2O2 and peroxiredoxin redox state—embedded in composite panels that pair flux with damage footprints and iron/ferroptosis metrics for attribution and trial guidance. Therapeutically, we argue against indiscriminate antioxidant loading in favor of node-specific, compartment-targeted modulation (NOX/NOS tuning, mitochondrial QC/RET tempering, ER redox control, iron/ferroptosis management, calibrated sulfur-axis support), implemented as time-staged sequences and titrated to biomarkers. Clarifying which species arise, where and when, reframes ROS from generic toxicity to precision redox modulation with translational impact.
Indexed as
Identifiers
What Socratic 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 Socratic graph.