Effect of Heparin on Viologen-Stimulated Enzymatic NADH Depletion

Zielonka, Jacek; Rybák, M.; Celińska, Joanna; Adamus, Jan; Marcinek, Andrzej; Gębicki, Jerzy

doi:10.1021/tx050336s

Cited by 13 publications

(6 citation statements)

References 44 publications

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“…xanthine oxidase by decreasing and regulating the concentration of this enzyme which reduces the production of reactive oxygen species in the endothelium (18)(19)(20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

Comparison of four pharmacological strategies aimed to prevent the lung inflammation and paraquat-induced alveolar damage

Rodriguez

Castro

Vela

et al. 2019

Preprint

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Objective : The aim of this study was to compare in vivo effect of five pharmacological options on inflammation and pulmonary fibrosis induced by paraquat. Methods: 54 Wistar SPF rats were used. After 2 hours post-intoxication with paraquat ion, groups of 9 animals were randomly assigned to : (1) cyclophosphamide plus dexamethasone (2) low molecular weight heparin (3) unfractionated heparin (4) vitamin C every 24 h , (v) atorvastatin or (vi) placebo with intraperitoneal saline .Lung inflammation, alveolar injury, hepatocyte damage, hepatic regeneration, acute tubular necrosis and kidney congestion were evaluated. Results: In the control group 100% of animals presented moderate and severe lung inflammation, while in the groups with atorvastatin and intratracheal heparin this proportion was lower (55.5% ; CI 26.6 – 81.3%) (p = 0.025). A lower degree of moderate or severe hepatic regeneration was evident in the treatment groups with atorvastatin (p = 0.009). In this study was demonstrated that statins and heparin may have a protective effect in the paraquat-induced destructive phase. More evidence are needed to evaluated of dose response effects of these drugs before to study in clinical trials.

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“…xanthine oxidase by decreasing and regulating the concentration of this enzyme which reduces the production of reactive oxygen species in the endothelium (18)(19)(20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

Comparison of four pharmacological strategies aimed to prevent the lung inflammation and paraquat-induced alveolar damage

Rodriguez

Castro

Vela

et al. 2019

Preprint

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“…This makes it a highly polar divalent cationic compound that is easily reduced to an unstable DQ +● . 51 Further reduction yields polyhydrobipyridyl derivatives and atmospheric oxygen regenerates DQ 2+ . The distance between the two nitrogen atoms is about 3.5 Å.…”

Section: Physical and Chemical Properties And Formulationsmentioning

confidence: 99%

“…92 These metabolic pathways occur mainly in the liver via cytochrome P450 enzymes, and all metabolites are more easily excreted through the urine. 51,91,94 Fuke et al 35 identified both DQ dipyridone and monopyridone in the serum of three DQ-poisoned patients, with dipyridone reaching up to 20% of DQ in one patient. In vitro studies suggested that the cecal microflora of the rat can metabolize DQ to the monopyridone.…”

Section: Metabolismmentioning

confidence: 99%

“…100 Absorbed DQ ion and metabolites are mainly eliminated via urine within 48 h, irrespective of the route of administration. 51,54 In an in vivo study performed with rats, after DQ gavage administration (45 mg DQ ion/kg body weight [bw]), the herbicide was excreted mostly unchanged in urine and feces (6% and 89% of dose, respectively), and its metabolite DQ monopyridone was present mainly in feces (5% of dose) and in a lesser extent in urine. Furthermore, urianalysis of rats after subcutaneous route of 10 mg DQ ion/kg bw revealed the presence of DQ (75%), DQ monopyridone (3%), and DQ dipyridone (6%).…”

Section: Eliminationmentioning

confidence: 99%

“…Of note, the efficacy of melatonin depend on the administered dose, as it can protect against DQ-induced acute hepatic and renal toxicity and reduce mortality due to oxidative stress at low concentrations, whereas at high doses it can exert pro-oxidant effects. 119,126,137 Polymeric sulfates such as heparin, 51 the potent iron chelator desferrioxamine 204 and the climbing plant Forsythia suspense 120 were also demonstrated to inhibit significantly the DQ-induced redox cycling procedures.…”

Section: Treatmentmentioning

confidence: 99%

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Human and experimental toxicology of diquat poisoning: Toxicokinetics, mechanisms of toxicity, clinical features, and treatment

2018

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Diquat (1,1′-ethylene-2,2′-bipyridinium ion; DQ) is a nonselective quick-acting herbicide, which is used as contact and preharvest desiccant to control terrestrial and aquatic vegetation. Several cases of human poisoning were reported worldwide mainly due to intentional ingestion of the liquid formulations. Its toxic potential results from its ability to produce reactive oxygen and nitrogen species through redox cycling processes that can lead to oxidative stress and potentially cell death. Kidney is the main target organ due to DQ toxicokinetics and redox cycling. There is no antidote against DQ intoxications, and the efficacy of treatments currently applied is still unsatisfactory. The aim of this work was to review the most relevant human and experimental findings related to DQ, characterizing its chemistry, activity as herbicide, mechanisms of toxicity, consequences of poisoning, and potential therapeutic approaches taking into account previous experience in developing antidotes for paraquat, a more toxic bipyridinium herbicide.

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Imaging Findings and Toxicological Mechanisms of Nervous System Injury Caused by Diquat

Ren,

Guo,

Wang

2024

Mol Neurobiol

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Diquat (DQ) is a nonselective bipyridine herbicide with a structure resembling paraquat (PQ). In recent years, the utilization of DQ as a substitute for PQ has grown, leading to an increase in DQ poisoning cases. While the toxicity mechanism of DQ remains unclear, it is primarily attributed to the intracellular generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) through the process of reduction oxidation. This results in oxidative stress, leading to a cascade of clinical symptoms. Notably, recent reports on DQ poisoning have highlighted a concerning trend: an upsurge in cases involving neurological damage caused by DQ poisoning. These patients often present with severe illness and a high mortality rate, with no effective treatment available thus far. Imaging findings from these cases have shown that neurological damage tends to concentrate on the brainstem. However, the specific mechanisms behind this poisoning remain unclear, and no specific antidote exists. This review summarizes the research progress on DQ poisoning and explores potential mechanisms. By shedding light on the nerve damage associated with DQ poisoning, we hope to raise awareness, propose new avenues for investigating the mechanisms of DQ poisoning, and lay the groundwork for the development of treatment strategies for DQ poisoning. Trial registration number: 2024PS174K.

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Effect of Heparin on Viologen-Stimulated Enzymatic NADH Depletion

Cited by 13 publications

References 44 publications

Comparison of four pharmacological strategies aimed to prevent the lung inflammation and paraquat-induced alveolar damage

Comparison of four pharmacological strategies aimed to prevent the lung inflammation and paraquat-induced alveolar damage

Human and experimental toxicology of diquat poisoning: Toxicokinetics, mechanisms of toxicity, clinical features, and treatment

Imaging Findings and Toxicological Mechanisms of Nervous System Injury Caused by Diquat

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