Acute diquat poisoning with intracerebral bleeding

Saeed, Saad; Wilks, Martin F.; Coupe, Michael

doi:10.1136/pmj.77.907.329

Cited by 31 publications

(24 citation statements)

References 16 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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“…These anions may react to form hydrogen peroxide and subsequently the highly reactive hydroxyl radical, which may then cause lipid peroxidation and cell death [ 159 , 160 ]. Another factor contributing to toxicity is the depletion of nicotinamide adenine dinucleotide phosphate with a bound hydrogen ion (NADPH), as both herbicide redox cycling and hydrogen peroxide detoxification via glutathione are NADPH dependent [ 159 , 161 ]. In addition to redox-cycling, there is some evidence that paraquat may be able to interact with enzymatic targets in the CNS, such as AChE and butylcholinesterase [ 162 ].…”

Section: Introductionmentioning

confidence: 99%

“…In severe and usually fatal cases of diquat poisoning, coma has also been reported [ 160 ]. Severe neurological and neuropsychiatric complications due to brain stem infarction and/or intracranial haemorrhage have also been described [ 161 , 163 , 166 ].…”

Section: Introductionmentioning

confidence: 99%

Potential developmental neurotoxicity of pesticides used in Europe

2008

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Pesticides used in agriculture are designed to protect crops against unwanted species, such as weeds, insects, and fungus. Many compounds target the nervous system of insect pests. Because of the similarity in brain biochemistry, such pesticides may also be neurotoxic to humans. Concerns have been raised that the developing brain may be particularly vulnerable to adverse effects of neurotoxic pesticides. Current requirements for safety testing do not include developmental neurotoxicity. We therefore undertook a systematic evaluation of published evidence on neurotoxicity of pesticides in current use, with specific emphasis on risks during early development. Epidemiologic studies show associations with neurodevelopmental deficits, but mainly deal with mixed exposures to pesticides. Laboratory experimental studies using model compounds suggest that many pesticides currently used in Europe -including organophosphates, carbamates, pyrethroids, ethylenebisdithiocarbamates, and chlorophenoxy herbicides -can cause neurodevelopmental toxicity. Adverse effects on brain development can be severe and irreversible. Prevention should therefore be a public health priority. The occurrence of residues in food and other types of human exposures should be prevented with regard to the pesticide groups that are known to be neurotoxic. For other substances, given their widespread use and the unique vulnerability of the developing brain, the general lack of data on developmental neurotoxicity calls for investment in targeted research. While awaiting more definite evidence, existing uncertainties should be considered in light of the need for precautionary action to protect brain development.

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“…Saeed S A M . (2001) also reported an intracerebral bleeding following acute paraquat ingestion (19). The report was based on a 52 year-old male who had ingested about 160 ml of "Weed killer".…”

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confidence: 99%