Evidence map›Paper›PMID 23826152›Full record

ArticlePloS one2013

P2X7 Cell Death Receptor Activation and Mitochondrial Impairment in Oxaliplatin-Induced Apoptosis and Neuronal Injury: Cellular Mechanisms and In Vivo Approach.

France Massicot, Guillaume Hache, Ludivine David, Dominique Chen, Charlotte Leuxe, Laure Garnier-Legrand, Patrice Rat, Olivier Laprévote, François Coudoré

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02169908 (LIPIDOXA, a Pilot Study of Analysis of Chronic Neuropathic Pain Markers in Patients Treated With Oxaliplatin-based Regimen), which is not on this map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 12% 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.

NCT02169908 nacompletednot on this mapstarted 2014, after this paper: background citation

LIPIDOXA, a Pilot Study of Analysis of Chronic Neuropathic Pain Markers in Patients Treated With Oxaliplatin-based Regimen

TypeinterventionalSponsorFondation Hôpital Saint-JosephRan2014 to 2016Enrolled35ConditionsDigestive Cancer, Gynecological CancerArmsThermotest, von Frey hairs
3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. The Role of Oxidative Stress in Peripheral Neuropathy.Journal of molecular neuroscience : MN · 2020
    Pooled it
  2. Review
  3. Ethanolic Extracts ofAdvances in pharmacological and pharmaceutical sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

France MassicotLaboratoire de Chimie-Toxicologie Analytique et Cellulaire, EA4463, Faculté des Sciences Pharmaceutiques et Biologiques, Université Paris Descartes, PRES Sorbonne Paris Cité, Paris, France.
Guillaume Hache
Ludivine David
Dominique Chen
Charlotte Leuxe
Laure Garnier-Legrand
Patrice Rat
Olivier Laprévote
François Coudoré
Sorbonne Paris Cité · FRLaboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Limited information is available regarding the cellular mechanisms of oxaliplatin-induced painful neuropathy during exposure of patients to this drug. We therefore determined oxidative stress in cultured cells and evaluated its occurrence in C57BL/6 mice. Using both cultured neuroblastoma (SH-SY5Y) and macrophage (RAW 264.7) cell lines and also brain tissues of oxaliplatin-treated mice, we investigated whether oxaliplatin (OXA) induces oxidative stress and apoptosis. Cultured cells were treated with 2-200 µM OXA for 24 h. The effects of pharmacological inhibitors of oxidative stress or inflammation (N-acetyl cysteine, ibuprofen, acetaminophen) were also tested. Inhibitors were added 30 min before OXA treatment and then in combination with OXA for 24 h. In SH-SY5Y cells, OXA caused a significant dose-dependent decrease in viability, a large increase in ROS and NO production, lipid peroxidation and mitochondrial impairment as assessed by a drop in mitochondrial membrane potential, which are deleterious for the cell. An increase in levels of negatively charged phospholipids such as cardiolipin but also phosphatidylserine and phosphatidylinositol, was also observed. Additionally, OXA caused concentration-dependent P2X7 receptor activation, increased chromatin condensation and caspase-3 activation associated with TNF-α and IL-6 release. The majority of these toxic effects were equally observed in Raw 264.7 which also presented high levels of PGE2. Pretreatment of SH-SY5Y cells with pharmacological inhibitors significantly reduced or blocked all the neurotoxic OXA effects. In OXA-treated mice (28 mg/kg cumulated dose) significant cold hyperalgesia and oxidative stress in the tested brain areas were shown. Our study suggests that targeting P2X7 receptor activation and mitochondrial impairment might be a potential therapeutic strategy against OXA-induced neuropathic pain.

Indexed as

AnimalsApoptosisBrainCell Line, TumorCell SurvivalDose-Response Relationship, DrugHumansMacrophagesMaleMice, Inbred C57BLMitochondriaNeuronsNeuroprotective AgentsOrganoplatinum CompoundsOxaliplatinOxidative StressNeuroprotective AgentsOrganoplatinum CompoundsOxaliplatinReceptors, Purinergic P2X7

Identifiers

PMID23826152
PMCPMC3695015
OpenAlexW1970393139

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.