Evidence map›Paper›PMID 18502740›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2008

Probing mechanisms of axonopathy. Part I: Protein targets of 1,2-diacetylbenzene, the neurotoxic metabolite of aromatic solvent 1,2-diethylbenzene.

Desire Tshala-Katumbay, Victor Monterroso, Robert Kayton, Michael Lasarev, Mohammad Sabri, Peter Spencer

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. On the biomarkers and mechanisms of konzo, a distinct upper motor neuron disease associated with food (cassava) cyanogenic exposure.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2011
    Article
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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

6 authors at 1 institution in 1 country.

Desire Tshala-KatumbayCenter for Research on Occupational and Environmental Toxicology, Oregon Health & Science University, 3181 S.W. Jackson Park Road, mail code L606, Portland, OR 97239, USA. tshalad@ohsu.edu
Victor Monterroso
Robert Kayton
Michael Lasarev
Mohammad Sabri
Peter Spencer
Oregon Health & Science University · US

Funding

NEUROTOXICOGENOMICS AND CHILD HEALTHU19ES011384 · NIEHS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SPENCER, PETER S · 2001 to 2006
$8.7M
TCE reductive dehalogenation by a microbial communityP42ES010338 · NIEHS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SPENCER, PETER S · 2000 to 2007
$8.2M
Toxic Probes of AxonopathyK01NS052183 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI TSHALA-KATUMBAY, DANIEL DESIRE · 2005 to 2009
$773k
NIEHS NIH HHS P42ES10338NIEHS NIH HHS U19ES11384NINDS NIH HHS K01 NS052183NINDS NIH HHS K01NS052183
6 · The paper itself

Abstract

Motor neuron axonopathy in diseases such as amyotrophic lateral sclerosis can be modeled and probed with neurotoxic chemicals that induce similar patterns of pathology, such as axonal spheroids that represent focal accumulation of anterogradely transported neurofilaments (NFs). The aromatic gamma-diketone-like 1,2-diacetylbenzene (1,2-DAB), but not its 1,3-DAB isomer, reacts with epsilon-amino- or sulfyhydryl groups of (neuro)proteins, forms adducts, and causes NFs to accumulate at proximal sites of elongate motor axons. We exploit the protein-reactive properties of neurotoxic 1,2-DAB versus the nonprotein-reactive properties of non-neurotoxic 1,3-DAB to unveil proteomic changes associated with this type of pathology. We used two-dimensional differential in-gel electrophoresis (2D-DIGE), matrix-assisted laser desorption/ionization time-of-flight tandem mass spectrometry to analyze the lumbosacral spinal cord proteome of adult Sprague-Dawley rats treated systemically with 20 mg/kg/day 1,2-DAB, equimolar dose of 1,3-DAB, or equivalent volume of vehicle (saline containing 2% acetone), 5 days a week, for 2 weeks. 1,2-DAB significantly altered the expression of protein disulfide isomerase, an enzyme involved in protein folding, and gelsolin, an actin-capping and -severing protein. Modifications of these two proteins have been incriminated in the pathogenesis of nerve fiber degeneration. Protein-reactive and neurotoxic 1,2-DAB appears to be excellent tool to dissect mechanisms of nerve fiber (axon) degeneration.

Indexed as

AcetophenonesAnimalsAxonsBenzene DerivativesBody WeightElectrophoresis, Gel, Two-DimensionalGelsolinMaleProtein Disulfide-IsomerasesProteomicsRatsRats, Sprague-DawleySpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationSpinal Cord1,2-diacetylbenzene1,2-diethylbenzeneAcetophenonesBenzene DerivativesGelsolinProtein Disulfide-Isomerases

Identifiers

PMID18502740
PMCPMC2734301
OpenAlexW2022353852

What OpenQuestion holds

Textmetadata
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.