Mechanisms of Toxicity, Clinical Features, and Management of Diquat Poisoning: A Review

Jones, G. Morgan; Vale, J. A.

doi:10.1081/clt-100100926

Cited by 199 publications

(172 citation statements)

References 28 publications

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“…However, PQ (but not MPTP or rotenone) is a potent redox cycler, readily converting to a free radical that interacts with molecular O 2 to generate superoxide anions and other ROS within mitochondria (51,120) (Fig. 8).…”

Section: Paraquat Metabolism and Mitochondrial Mechanisms Of Neurotoxmentioning

confidence: 99%

Toxin Models of Mitochondrial Dysfunction in Parkinson's Disease

Martinez

Greenamyre

2012

Antioxidants & Redox Signaling

229

155

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Significance: Parkinson's disease (PD) is a neurodegenerative disorder characterized, in part, by the progressive and selective loss of dopaminergic neuron cell bodies within the substantia nigra pars compacta (SNpc) and the associated deficiency of the neurotransmitter dopamine (DA) in the striatum, which gives rise to the typical motor symptoms of PD. The mechanisms that contribute to the induction and progressive cell death of dopaminergic neurons in PD are multi-faceted and remain incompletely understood. Data from epidemiological studies in humans and molecular studies in genetic, as well as toxin-induced animal models of parkinsonism, indicate that mitochondrial dysfunction occurs early in the pathogenesis of both familial and idiopathic PD. In this review, we provide an overview of toxin models of mitochondrial dysfunction in experimental Parkinson's disease and discuss mitochondrial mechanisms of neurotoxicity. Recent Advances: A new toxin model using the mitochondrial toxin trichloroethylene was recently described and novel methods, such as intranasal exposure to toxins, have been explored. Additionally, recent research conducted in toxin models of parkinsonism provides an emerging emphasis on extranigral aspects of PD pathology. Critical Issues: Unfortunately, none of the existing animal models of experimental PD completely mimics the etiology, progression, and pathology of human PD. Future Directions: Continued efforts to optimize established animal models of parkinsonism, as well as the development and characterization of new animal models are essential, as there still remains a disconnect in terms of translating mechanistic observations in animal models of experimental PD into bona fide diseasemodifying therapeutics for human PD patients. Antioxid. Redox Signal. 16, 920-934.

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Section: Paraquat Metabolism and Mitochondrial Mechanisms Of Neurotoxmentioning

confidence: 99%

Toxin Models of Mitochondrial Dysfunction in Parkinson's Disease

Martinez

Greenamyre

2012

Antioxidants & Redox Signaling

229

155

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“…5 The clinical manifestations range from local irritation to multiple-organ failure and death. Systemic manifestations depend on the amount ingested, and patients can be classified into 3 categories (Table 3).…”

Section: Resultsmentioning

confidence: 99%

Clinical spectrum and outcome of paraquat poisoning in a tertiary care teaching hospital

Halesha

Venugopal

2018

Int J Adv Med

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Background: Paraquat is most common insecticide compound used for suicidal consumption in rural part of the Karnataka next to organo-phosphorous compound. It produces various local and systemic manifestations in the early course. It is very notorious to cause multi-organ dysfunction and mortality within 24 hours in severe amount of consumption. Lack of specific antidote and high-quality evidence based medicine makes the management of paraquat poisoning challenging. Hence, we took up the study to evaluate the clinical features, course and management option for the poisoning.Methods: It is an observational study conducted at HIMS, Hassan. History was collected from patient and bystanders. Clinical features, laboratory parameters were noted regularly and frequently. Patient’s complications were identified initially and treated accordingly. All the data collected were tabulated and statistically analysed.Results: Out of 110 patients, 72 were females and 38 were males; most of them were in the age group of 30-40 years. Mild poisoning was noted in 30, moderate in 56 and 24 patients were severe. Most common symptom was nausea and signs were oral cavity ulcers followed by tachycardia and tachypnoea. The overall mortality was 72%, 18% were recovered fully and 10% patients left against medical advice.Conclusions: Since there is a lack of antidote management of paraquat is challenging. Early gastric lavage, aggressive fluids, IV methyl prednisolone and N-Acetyl-Cysteine is beneficial.

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“…However, the mortality rate of PQ poisoning has been reported to range from 50 to 90% when the pesticide is ingested either accidentally or intentionally as a suicide attempt (1). A previous study suggested that absorbed PQ requires removal from the bloodstream in order to improve the survival rate of patients with severe PQ poisoning (2).…”

Section: Introductionmentioning

confidence: 99%