ArticleCardiovascular toxicology2017
Environmentally Persistent Free Radicals Cause Apoptosis in HL-1 Cardiomyocytes.
Article in Cardiovascular toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 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
- pH-Dependent Activation of EPFRs and Kinetics of Hydroxyl Radical Generation.Environmental science & technology · 2026Article
- Oxidative potential and persistent free radicals in dust storm particles and their associations with hospitalization.Nature communications · 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
- Biochar-Derived Persistent Free Radicals: A Plethora of Environmental Applications in a Light and Shadows Scenario.Toxics · 2024Review
- Phytochemical composition and antioxidant activities of some wild edible plants locally consumed by rural communities in northern Uganda.Frontiers in nutrition · 2023Article
- Suppressive Effects ofPharmaceuticals (Basel, Switzerland) · 2022Article
- CBL knockdown protects cardiomyocytes against hypoxia-reoxygenation injury by downregulating GRB2 expression.Experimental and therapeutic medicine · 2022Article
- A critical review of environmentally persistent free radical (EPFR) solvent extraction methodology and retrieval efficiency.Chemosphere · 2021Review
- 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
- Selenium Polysaccharide SPMP-2a fromBioMed research international · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Samples of environmental particulate matter contain environmentally persistent free radicals (EPFRs) capable of sustained generation of oxygen radicals. While exposure to EPFRs produces cardiac toxicity and oxidative stress in experimental animals, the underlying mechanisms are largely unknown. To determine whether EPFRs could directly damage cardiomyocytes, cultured mouse cardiomyocytes (HL-1) and primary rat adult left ventricular myocytes (ALVM) were incubated with an EPFR consisting of 1,2-dichlorobenzene chemisorbed to CuO-coated silica beads (DCB230). Treatment with DCB230 killed both HL-1 and ALVM in a dose- and time-dependent manner. The cytotoxic effects of DCB230 were significantly attenuated by treatment with α-tocopherol. One to 2 h after exposure to DCB230, there were significant reductions in mitochondrial membrane potential and significant increases in cleaved caspase-9, but no significant increases in DNA damage or cell death. After 8 h of treatment, there were significant increases in caspase-3, caspase-9, DNA damage and PARP cleavage associated with significant cell death. Together, these data indicate that DCB230 kills HL-1 myocytes by inducing oxidative stress that initiates apoptosis, with the intrinsic or mitochondrial pathway acting early in the apoptotic signaling process.
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.