ArticleJournal of receptor and signal transduction research2011
Environmentally persistent free radicals decrease cardiac function before and after ischemia/reperfusion injury in vivo.
Article in Journal of receptor and signal transduction research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- A systematic review of environmentally persistent free radical (EPFR) formation, characteristics, and health effects: are there sufficient data for risk assessment?Journal of toxicology and environmental health. Part B, Critical reviews · 2026Pooled it
- Understanding the influence of environmentally persistent free radical location on reactive oxygen species generation in soils.Chemosphere · 2026Article
- Spatial distribution of persistent components of particulate matter near a hazardous waste thermal treatment facility.Environmental pollution (Barking, Essex : 1987) · 2026Article
- Persistent chemicals in particulate matter (PM) near a hazardous waste thermal treatment facility.Atmospheric pollution research · 2025Article
- From smog to scarred hearts: unmasking the detrimental impact of air pollution on myocardial ischemia-reperfusion injury.Cellular and molecular life sciences : CMLS · 2025Review
- Environmentally persistent free radicals lead to selective inhibition of CYP1 monooxygenase activities, and increased production of reactive oxygen species by reaction uncoupling.Frontiers in public health · 2025Article
- The Effect of α-FeToxics · 2024Article
- Inhalation of particulate matter containing environmentally persistent free radicals induces endothelial dysfunction mediated via AhR activation at the air-blood interface.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Role of Electronegativity in Environmentally Persistent Free Radicals (EPFRs) Formation on ZnO.The journal of physical chemistry. C, Nanomaterials and interfaces · 2024Article
- A critical review of environmentally persistent free radical (EPFR) solvent extraction methodology and retrieval efficiency.Chemosphere · 2021Review
- Formation of Environmentally Persistent Free Radicals (EPFRs) on the Phenol-DosedThe journal of physical chemistry. C, Nanomaterials and interfaces · 2021Article
- Inhalation of particulate matter containing free radicals leads to decreased vascular responsiveness associated with an altered pulmonary function.American journal of physiology. Heart and circulatory physiology · 2021Article
- Developmental Hazard of Environmentally Persistent Free Radicals and Protective Effect of TEMPOL in Zebrafish Model.Toxics · 2021Article
- Cardioprotective effects of garcinol following myocardial infarction in rats with isoproterenol-induced heart failure.AMB Express · 2020Article
- Ecological risk analysis of the solid residues collected from the thermal disposal process of hyperaccumulator Pteris vittata including heavy metals and environmentally persistent free radicals.Environmental science and pollution research international · 2019Article
- Environmentally Persistent Free Radicals: Insights on a New Class of Pollutants.Environmental science & technology · 2018Article
- Unraveling mechanisms of toxicant-induced oxidative stress in cardiovascular disease.Current opinion in toxicology · 2018Article
- A Scalable Field Study Protocol and Rationale for Passive Ambient Air Sampling: A Spatial Phytosampling for Leaf Data Collection.Environmental science & technology · 2017Article
- Environmentally Persistent Free Radicals Cause Apoptosis in HL-1 Cardiomyocytes.Cardiovascular toxicology · 2017Article
- Formation of environmentally persistent free radicals (EPFRs) on ZnO at room temperature: Implications for the fundamental model of EPFR generation.Chemical physics letters · 2017Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Exposure to airborne particles is associated with increased cardiovascular morbidity and mortality. During the combustion of chlorine-containing hazardous materials and fuels, chlorinated hydrocarbons chemisorb to the surface of transition metal-oxide-containing particles, reduce the metal, and form an organic free radical. These radical-particle systems can survive in the environment for days and are called environmentally persistent free radicals (EPFRs). This study determined whether EPFRs could decrease left ventricular function before and after ischemia and reperfusion (I/R) in vivo. Male Brown-Norway rats were dosed (8 mg/kg, intratracheal) 24 h prior to testing with particles containing the EPFR of 1, 2-dichlorobenzene (DCB230). DCB230 treatment decreased systolic and diastolic function. DCB230 also produced pulmonary and cardiac inflammation. After ischemia, systolic, but not diastolic function was significantly decreased in DCB230-treated rats. Ventricular function was not affected by I/R in control rats. There was greater oxidative stress in the heart and increased 8-isoprostane (biomarker of oxidative stress) in the plasma of treated vs. control rats after I/R. These data demonstrate for the first time that DCB230 can produce inflammation and significantly decrease cardiac function at baseline and after I/R in vivo. Furthermore, these data suggest that EPFRs may be a risk factor for cardiac toxicity in healthy individuals and individuals with ischemic heart disease. Potential mechanisms involving cytokines/chemokines and/or oxidative stress are discussed.
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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.