Evidence map›Paper›PMID 27027721›Full record

ArticlePediatric research2016

Toluene disruption of the functions of L1 cell adhesion molecule at concentrations associated with occupational exposures.

Kimberly M R White, Julia A Sabatino, Min He, Natalie Davis, Ningfeng Tang, Cynthia F Bearer

Abstract read
In one paragraph

Article in Pediatric research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Kimberly M R WhiteDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland.
Julia A SabatinoDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland.
Min HeDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland.
Natalie DavisDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland.
Ningfeng TangDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland.
Cynthia F BearerDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland.

Funding

The Role of Lipid Rafts in Fetal Alcohol Spectrum DisorderR01AA016398 · NIAAA · UNIVERSITY OF MARYLAND BALTIMORE · PI BEARER, CYNTHIA FRANCES · 2007 to 2011
$1.5M
NIAAA NIH HHS R01 AA016398
6 · The paper itself

Abstract

backgroundPrenatal toluene exposure can cause neurodevelopmental disabilities similar to fetal alcohol syndrome. Both share neuroanatomic pathologies similar to children with mutations in L1 cell adhesion molecule (L1). L1 mediates neurite outgrowth (NOG) via signaling through ERK1/2, which require trafficking of L1 through lipid rafts. Our objective is to determine if toluene inhibits L1-mediated NOG and toluene inhibits L1 signaling at concentrations achieved during occupational exposure.

methodsConcentrations of toluene reflective of blood concentrations achieved in solvent abusers and occupational settings are used. Cerebellar granule neurons (CGN) harvested from postnatal day 6 rat pups are plated on coverslips coated with poly-L-lysine (PLL) alone or PLL followed by laminin. L1 is added to the media of CGN plated on PLL alone. Toluene is added 2 h after plating. Cells are fixed at 24 h and neurite length is measured. ERK1/2 activation by L1 in CGN is analyzed by immunoblot.

resultsToluene significantly reduced mean neurite length of CGN exposed to L1 but not laminin. Toluene significantly reduced L1-mediated ERK1/2 phosphorylation.

conclusionResults suggest that toluene inhibits L1-lipid raft interactions at occupationally relevant concentrations and may lead to a fetal solvent spectrum disorder similar to fetal alcohol spectrum disorder.

Indexed as

AnimalsExtracellular Signal-Regulated MAP KinasesFemaleLamininMaternal ExposureMembrane MicrodomainsNeural Cell Adhesion Molecule L1NeuritesNeuronsOccupational ExposurePhosphorylationPregnancyPrenatal Exposure Delayed EffectsRatsRats, Sprague-DawleyTolueneExtracellular Signal-Regulated MAP KinasesLamininNeural Cell Adhesion Molecule L1Toluene

Identifiers

PMID27027721
PMCPMC4929035

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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.