Observational studyClinical toxicology (Philadelphia, Pa.)2017
A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells.
Observational study in Clinical toxicology (Philadelphia, Pa.), 2017. 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
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Targeting Mitochondrial Dysfunction in Acute Organophosphate Toxicity: A Preliminary Evaluation of Cyclosporine A.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2026Article
- Mitochondrial dysfunction, cerebral metabolic crisis, and exploratory bioenergetic biomarkers in a translational swine model of acute carbon monoxide poisoning.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Attenuation of mitochondrial dysfunction in a ventricular fibrillation swine model of cardiac arrest treated with carbon monoxide.Resuscitation · 2025Article
- Blood Cells as a Cellular Biomarker for Mitochondrial Function in a Experimental Model of Acute Carbon Monoxide Poisoning with Treatment.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2025Article
- The histone modification regulator, SIN3, plays a role in the cellular response to changes in glycolytic flux.PloS one · 2025Article
- Investigation of Cerebral Mitochondrial Injury in a Porcine Survivor Model of Carbon Monoxide Poisoning.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2024Article
- Assessing Platelet Mitochondrial Dysfunction in a Murine Model of Acute Acetaminophen Toxicity.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2023Article
- Alterations in cerebral and cardiac mitochondrial function in a porcine model of acute carbon monoxide poisoning.Clinical toxicology (Philadelphia, Pa.) · 2021Article
- Emerging cellular-based therapies in carbon monoxide poisoning.American journal of physiology. Cell physiology · 2021Review
- Ex vivo use of cell-permeable succinate prodrug attenuates mitochondrial dysfunction in blood cells obtained from carbon monoxide-poisoned individuals.American journal of physiology. Cell physiology · 2020Article
- Prophylaxis of mitochondrial dysfunction caused by cellular decompression from hyperbaric exposure.Mitochondrion · 2020Article
- In vitro comparison of hydroxocobalamin (B12a) and the mitochondrial directed therapy by a succinate prodrug in a cellular model of cyanide poisoning.Toxicology reports · 2020Article
- Review
- Thermal-Responsive Carbon Monoxide (CO) Delivery Expedites Metabolic Exhaustion of Cancer Cells toward Reversal of Chemotherapy Resistance.ACS central science · 2019Article
- Mitochondrial networking in human blood cells with application in acute care illnesses.Mitochondrion · 2019Article
- Acute decompression following simulated dive conditions alters mitochondrial respiration and motility.American journal of physiology. Cell physiology · 2018Article
- Translational Application of Measuring Mitochondrial Functions in Blood Cells Obtained from Patients with Acute Poisoning.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2018Article
- Alterations in mitochondrial respiration and reactive oxygen species in patients poisoned with carbon monoxide treated with hyperbaric oxygen.Intensive care medicine experimental · 2018Article
- Mitochondrial dynamics and respiration within cells with increased open pore cytoskeletal meshes.Biology open · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesCarbon monoxide (CO) is a colorless and odorless gas responsible for poisoning mortality and morbidity in the United States. At this time, there is no reliable method to predict the severity of poisoning or clinical prognosis following CO exposure. Whole blood cells, such as peripheral blood mononuclear cells (PBMCs) and platelets, have been explored for their potential use to act as sensitive biomarkers for mitochondrial dysfunction which may have a role in CO poisoning.
designThe objective of this study was to measure mitochondrial respiration using intact cells obtained from patients exposed to CO as a potential biomarker for mitochondrial inhibition with results that can be obtained in a time frame useful for guiding clinical care. This was a prospective, observational pilot study performed from July 2015 to July 2016 at a single academic tertiary care center that is the location of the region's only multi chamber hyperbaric. MEASUREMENTS: Clinical characteristics, patient demographics, mitochondrial respiration and outcomes were recorded. MAIN
resultsThere were 7 patients enrolled with a mean COHb level 26.8 ± 10 and with a mean lactate of 1.1 ± 0.4 mmol/L. All 7 CO exposures were related to heat generators used during winter months with two deaths. There was a positive correlation between maximal respiration and COHb levels with both high maximal respiration and high spare respiratory capacity correlating with a high COHb level. There was a subset of PBMCs (n = 4) that were analyzed for Complex IV (cytochrome c oxidase) activity.
conclusionsIn this pilot study, measurements can be performed in an appropriate timeline for clinical care with potential to serve as a prognostic marker. Further work is necessary to develop high-resolution respirometry as a clinical tool for assessing the severity of illness and guiding therapy.
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