ArticleScientific reports2022
Succinate prodrugs in combination with atropine and pralidoxime protect cerebral mitochondrial function in a rodent model of acute organophosphate poisoning.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Optical and Microdialysis Monitoring of Succinate Prodrug Treatment in a Rotenone-Induced Model of Mitochondrial Dysfunction in Swine.Metabolites · 2026Article
- Neuroprotective Effects of N-Acetylcysteine-Amide (AD4) in a Survival Mouse Model of Paraoxon Intoxication: Targeting Oxidative Stress, Neuroinflammation and Memory Impairments.Antioxidants (Basel, Switzerland) · 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
- Redirecting Intermediary Metabolism to Counteract Cyanide Poisoning.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Recent Development of Nanoparticle Platforms for Organophosphate Nerve Agent Detoxification.Langmuir : the ACS journal of surfaces and colloids · 2025Review
- Current Trends in Clinical Trials of Prodrugs.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Susceptibility to radiation adverse effects in veterans with Gulf War illness and healthy civilians.Scientific reports · 2024Article
- Cell-Free DNA as a Biomarker in a Rodent Model of Chlorpyrifos Poisoning Causing Mitochondrial Dysfunction.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2023Article
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Pesticides account for hundreds of millions of cases of acute poisoning worldwide each year, with organophosphates (OPs) being responsible for the majority of all pesticide-related deaths. OPs inhibit the enzyme acetylcholinesterase (AChE), which leads to impairment of the central- and peripheral nervous system. Current standard of care (SOC) alleviates acute neurologic-, cardiovascular- and respiratory symptoms and reduces short term mortality. However, survivors often demonstrate significant neurologic sequelae. This highlights the critical need for further development of adjunctive therapies with novel targets. While the inhibition of AChE is thought to be the main mechanism of injury, mitochondrial dysfunction and resulting metabolic crisis may contribute to the overall toxicity of these agents. We hypothesized that the mitochondrially targeted succinate prodrug NV354 would support mitochondrial function and reduce brain injury during acute intoxication with the OP diisopropylfluorophosphate (DFP). To this end, we developed a rat model of acute DFP intoxication and evaluated the efficacy of NV354 as adjunctive therapy to SOC treatment with atropine and pralidoxime. We demonstrate that NV354, in combination with atropine and pralidoxime therapy, significantly improved cerebral mitochondrial complex IV-linked respiration and reduced signs of brain injury in a rodent model of acute DFP exposure.
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