ArticleNeurochemical research2012
Investigate the chronic neurotoxic effects of diquat.
Article in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 33 citations in OpenAlex.
- Molecular mechanisms in diquat-induced organs injury:insights into cell signaling and potential therapeutic agents.Cell biology and toxicology · 2025Review
- Diquat Induces Cell Death and dopamine Neuron Loss via Reactive Oxygen Species Generation inEnvironmental science & technology · 2025Article
- Lethal diquat poisoning manifests as acute central nervous system injury and circulatory failure: A retrospective cohort study of 50 cases.EClinicalMedicine · 2022Article
- Effects of Acute Diquat Poisoning on Liver Mitochondrial Apoptosis and Autophagy in Ducks.Frontiers in veterinary science · 2021Article
- Paraoxonase Role in Human Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Effects of Dual Exposure to the Herbicides Atrazine and Paraquat on Adult Climbing Ability and Longevity inInsects · 2019Article
- LRRK2 G2019S transgenic mice display increased susceptibility to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mediated neurotoxicity.Journal of chemical neuroanatomy · 2016Article
- Mitochondrial mechanisms of redox cycling agents implicated in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic exposure to agricultural chemicals (pesticides/herbicides) has been shown to induce neurotoxic effects or results in accumulation of various toxic metabolic by-products. These substances have the relevant ability to cause or increase the risk for neurodegeneration. Diquat is an herbicide that has been extensively used in the United States of America and other parts of the world. Diquat is constantly released into the environment during its use as a contact herbicide. Diquat structurally resembles 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) and paraquat. Rotenone, paraquat, maneb and MPTP reproduce features of movement disorders in experimental animal models. Based on the structural similarity to other neurotoxins, chronic exposure of diquat can induce behavioral and neurochemical alterations associated with dopaminergic neurotoxicity. However, in the present study, diquat unlike other neurotoxins (rotenone, 6-hydroxydopamine, MPTP, paraquat and maneb) did not induce dopamine depletion in the mouse striatum. Although, notable exacerbation in motor impairment (swimming score, akinesia and open field) were evident that may be due to the decreased dopamine turnover and mild nigrostriatal neurodegeneration. These data indicate that, despite the apparent structural similarity to other dopaminergic neurotoxins, diquat did not exert severe deleterious effects on dopamine neurons in a manner that is unique to rotenone and MPTP.
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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.