Fatal diquat intoxication

Jovic-Stosic, Jasmina; Stanković-Babić, Gordana; Todorović, Vladimir S.

doi:10.2298/vsp0906477j

Cited by 21 publications

(16 citation statements)

References 19 publications

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“…The herbicide diquat, which is structurally similar to paraquat, has replaced paraquat where its use has been prohibited due to a suggested association with Parkinson’s disease (McCormack et al 2002 ) and is now in widespread use as an agricultural and home use herbicide. Diquat is known to be toxic acutely in high doses (Hantson et al 2000 ; Jones and Vale 2000 ; Jovic-Stosic et al 2009 ; Saeed et al 2001 ; Schmidt et al 1999 ) and evidence of Parkinsonism after use of diquat has been suggested (Sechi et al 1992 ). Acutely, diquat causes intracerebral haemorrhage particularly in the white matter but also in the brainstem with a necrotic appearance (Vanholder et al 1981 ).…”

Section: Introductionmentioning

confidence: 99%

Diquat causes caspase-independent cell death in SH-SY5Y cells by production of ROS independently of mitochondria

Nisar

Hanson

et al. 2015

Arch Toxicol

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Evidence indicates that Parkinson’s disease (PD), in addition to having a genetic aetiology, has an environmental component that contributes to disease onset and progression. The exact nature of any environmental agent contributing to PD is unknown in most cases. Given its similarity to paraquat, an agrochemical removed from registration in the EU for its suspected potential to cause PD, we have investigated the in vitro capacity of the related herbicide Diquat to cause PD-like cell death. Diquat showed greater toxicity towards SH-SY5Y neuroblastoma cells and human midbrain neural cells than paraquat and also MPTP, which was independent of dopamine transporter-mediated uptake. Diquat caused cell death independently of caspase activation, potentially via RIP1 kinase, with only a minor contribution from apoptosis, which was accompanied by enhanced reactive oxygen species production in the absence of major inhibition of complex I of the mitochondrial respiratory chain. No changes in α-synuclein expression were observed following 24-h or 4-week exposure. Diquat may, therefore, kill neural tissue by programmed necrosis rather than apoptosis, reflecting the pathological changes seen following high-level exposure, although its ability to promote PD is unclear.

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Section: Introductionmentioning

confidence: 99%

Diquat causes caspase-independent cell death in SH-SY5Y cells by production of ROS independently of mitochondria

Nisar

Hanson

et al. 2015

Arch Toxicol

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“…The combined poisoning with diquat and glyphosate may cause severe mucosal damage including edema and hemorrhage. [4,5,17,21] Central nervous system symptoms include coma, epileptic seizures, and hemorrhage. [4,22] Shock and malignant arrhythmia may also occur in some cases.…”

Section: Discussionmentioning

confidence: 99%

“…Ingestion of diquat and herbicides may cause severe and fatal poisoning. [1,3–5] Because of a lack of an antidote, the development of respiratory failure, renal failure, hypotension, and multi-organ dysfunction syndrome (MODS) is highly associated with poor prognosis. [6–9] As a technology capable of providing short-term mechanical support to the lungs, extracorporeal membrane pulmonary oxygenation (ECMO) was associated with reduced mortality in patients with very severe acute respiratory distress syndrome (ARDS).…”

Section: Introductionmentioning

confidence: 99%

Successful extracorporeal membrane oxygenation support for severe acute diquat and glyphosate poisoning

Wang

Zhang

et al. 2019

Medicine

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Rationale: Because of the lack of an antidote or effective treatment, patients with severe acute diquat and glyphosate poisoning always died within a few hours. Extracorporeal membrane pulmonary oxygenation (ECMO), as an artificial heart-lung supporting system, can be applied to support lung that is expected to recover from reversible pathological damage. However, to our knowledge, the application of ECMO for patients with diquat and glyphosate poisoning has not been reported. Patient concerns: A 40-year-old man ingested in 100 ml of diquat (20 g/100 ml) and 400 ml glyphosate (41 g/100 ml) was admitted to the intensive care unit (ICU), immediately complicated by the development of ventricular fibrillation, respiratory failure, renal failure, and multi-organ failure. Diagnosis: Diquat and glyphosate poisoning were diagnosed by stated ingestion history, and the diagnostic criteria for acute respiratory distress syndrome (ARDS) and multi-organ dysfunction syndrome were also met. Interventions: He was treated with veno-venous ECMO. Outcomes: He was successfully transferred out of the ICU on day 46 and discharged on day 67. The computed tomography scan showed no obvious pulmonary fibrosis 2 months after poisoning. Lessons: ECMO may be effective in the treatment of patients with severe ARDS caused by diquat and glyphosate poisoning when conventional management does not work.

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“…Currently, there is no antidote or effective treatment for DQ intoxications, the treatment being devoted to reduce absorption and/or enhance elimination. 48,50 Because DQ does not accumulate in the lungs, intensive care treatment is likely to lead to a better prognosis than PQ.…”

Section: Treatmentmentioning

confidence: 99%

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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Fatal diquat intoxication

Abstract: Cardiocirculatory disturbances led to fatal complications, the heart and brain infarction. We pointed out the heart as one of the most severely affected organs in diquat poisoning.

Cited by 21 publications

References 19 publications

Diquat causes caspase-independent cell death in SH-SY5Y cells by production of ROS independently of mitochondria

Diquat causes caspase-independent cell death in SH-SY5Y cells by production of ROS independently of mitochondria

Successful extracorporeal membrane oxygenation support for severe acute diquat and glyphosate poisoning

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

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