Evidence map›Paper›PMID 25693864›Full record

ArticleArchives of toxicology2015

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

R Nisar, P S Hanson, L He, R W Taylor, P G Blain, C M Morris

Erratum issuedOpen access · hybridAbstract readComparative Study
In one paragraph

Article in Archives of toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

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  15. Vitamin DOxidative medicine and cellular longevity · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

R NisarThe Medical Toxicology Centre, and NIHR HPRU in Chemical and Radiation Threats and Hazards, Wolfson Building, Newcastle University, Claremont Place, Newcastle upon Tyne, Tyne and Wear, NE2 4AA, UK.
P S HansonThe Medical Toxicology Centre, and NIHR HPRU in Chemical and Radiation Threats and Hazards, Wolfson Building, Newcastle University, Claremont Place, Newcastle upon Tyne, Tyne and Wear, NE2 4AA, UK.
L HeMitochondrial Research Group, Institute of Neuroscience, The Medical School, Newcastle University, Framlington Place, Newcastle upon Tyne, Tyne and Wear, NE2 4HH, UK.
R W TaylorMitochondrial Research Group, Institute of Neuroscience, The Medical School, Newcastle University, Framlington Place, Newcastle upon Tyne, Tyne and Wear, NE2 4HH, UK.
P G BlainThe Medical Toxicology Centre, and NIHR HPRU in Chemical and Radiation Threats and Hazards, Wolfson Building, Newcastle University, Claremont Place, Newcastle upon Tyne, Tyne and Wear, NE2 4AA, UK.
C M MorrisThe Medical Toxicology Centre, and NIHR HPRU in Chemical and Radiation Threats and Hazards, Wolfson Building, Newcastle University, Claremont Place, Newcastle upon Tyne, Tyne and Wear, NE2 4AA, UK. c.m.morris@ncl.ac.uk.
Newcastle University · GB

Funding

Medical Research Council MR/K000608/1Wellcome Trust 096919
6 · The paper itself

Abstract

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.

Indexed as

ApoptosisCell DeathCell LineCell Line, TumorDiquatHerbicidesHumansMitochondriaMPTP PoisoningNecrosisNeural Stem CellsNeuroblastomaParaquatReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesTime FactorsDiquatHerbicidesParaquatReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesApoptosisDiquatMitochondriaNecrosisParkinson’s diseasePesticide

Identifiers

PMID25693864
PMCPMC4572080
OpenAlexW2056875060

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.