ArticleFree radical biology & medicine2011
Redox cycling and increased oxygen utilization contribute to diquat-induced oxidative stress and cytotoxicity in Chinese hamster ovary cells overexpressing NADPH-cytochrome P450 reductase.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 94 citations in OpenAlex.
- A rare intravenous paraquat exposure presenting with novel and atypical severe clinical manifestations.Indian journal of pharmacology · 2026Article
- Optimization of ultrasonic-assisted extraction of total saponins from Semen Ziziphi Spinosae and evaluation of their antioxidant activity and pH stability.Ultrasonics sonochemistry · 2026Article
- Effect of yeast selenium on autophagy and PINK1/Parkin expression in Diquat-induced chicken liver and kidney cells.Poultry science · 2026Article
- Enhanced Protective Potential of a Pea Protein-Fortified Fermented Almond Beverage Against Paraquat-Induced Oxidative Stress.Molecular nutrition & food research · 2026Article
- Intranasal curcumin mitigates paraquat-induced oxidative lung damage via involvement of neutrophil extracellular traps (NETs) in mice model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Tea tree oil attenuates diquat-induced hepatotoxicity in chickens via suppression of the NF-κB-mediated inflammatory pathway.Veterinary research communications · 2026Article
- Comparative investigation of the potential of glyphosate and glyphosate-based formulations to cause oxidative stress and DNA damage in human skin and liver cell systems.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Transcranial microtesla magnetic fields suppress neuroinflammation and neuronal oxidative stress burden.iScience · 2026Article
- Diquat-induced organ toxicity: a focus on regulated cell death pathways and mitochondrial dysfunction.Frontiers in cell and developmental biology · 2026Review
- Protective effects ofFrontiers in pharmacology · 2026Article
- Boric acid and quercetin supplementations alleviated paraquat-induced neurotoxic and irritation effects in human SH-SY5Y cells and in ovo models.BMC complementary medicine and therapies · 2025Article
- Molecular mechanisms in diquat-induced organs injury：insights into cell signaling and potential therapeutic agents.Cell biology and toxicology · 2025Review
- Diquat based herbicide impair the development and behavior of zebrafish embryos and larvae.Scientific reports · 2025Article
- Analysis of clinical characteristics and factors of central nervous system damage caused by acute bipyridine herbicide poisoning.iScience · 2025Article
- The G311E Mutant Gene of MATE Family Protein DTX6 Confers Diquat and Paraquat Resistance in Rice Without Yield or Nutritional Penalties.International journal of molecular sciences · 2025Article
- Effect of Diquat on gut health: molecular mechanisms, toxic effects, and protective strategies.Frontiers in pharmacology · 2025Review
- Case report: A case of acute renal failure, rhabdomyolysis, and toxic encephalopathy associated with diquat poisoning in a pregnant woman.Frontiers in medicine · 2025Article
- Imaging Findings and Toxicological Mechanisms of Nervous System Injury Caused by Diquat.Molecular neurobiology · 2024Review
- Thinking Induced by Acute Kidney Injury of Diquat Poisoning: Cases Report.Clinical medicine insights. Case reports · 2024Article
- Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
Diquat and paraquat are nonspecific defoliants that induce toxicity in many organs including the lung, liver, kidney, and brain. This toxicity is thought to be due to the generation of reactive oxygen species (ROS). An important pathway leading to ROS production by these compounds is redox cycling. In this study, diquat and paraquat redox cycling was characterized using human recombinant NADPH-cytochrome P450 reductase, rat liver microsomes, and Chinese hamster ovary (CHO) cells constructed to overexpress cytochrome P450 reductase (CHO-OR) and wild-type control cells (CHO-WT). In redox cycling assays with recombinant cytochrome P450 reductase and microsomes, diquat was 10-40 times more effective at generating ROS compared to paraquat (K(M)=1.0 and 44.2μM, respectively, for H(2)O(2) generation by diquat and paraquat using recombinant enzyme, and 15.1 and 178.5μM, respectively for microsomes). In contrast, at saturating concentrations, these compounds showed similar redox cycling activity (V(max)≈6.0nmol H(2)O(2)/min/mg protein) for recombinant enzyme and microsomes. Diquat and paraquat also redox cycle in CHO cells. Significantly more activity was evident in CHO-OR cells than in CHO-WT cells. Diquat redox cycling in CHO cells was associated with marked increases in protein carbonyl formation, a marker of protein oxidation, as well as cellular oxygen consumption, measured using oxygen microsensors; greater activity was detected in CHO-OR cells than in CHO-WT cells. These data demonstrate that ROS formation during diquat redox cycling can generate oxidative stress. Enhanced oxygen utilization during redox cycling may reduce intracellular oxygen available for metabolic reactions and contribute to toxicity.
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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.