Evidence map›Paper›PMID 28667285›Full record

ArticleScientific reports2017

Oxidative Stress Challenge Uncovers Trichloroacetaldehyde Hydrate-Induced Mitoplasticity in Autistic and Control Lymphoblastoid Cell Lines.

Richard Eugene Frye, Shannon Rose, Rebecca Wynne, Sirish C Bennuri, Sarah Blossom, Kathleen M Gilbert, Lynne Heilbrun, Raymond F Palmer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Richard Eugene FryeArkansas Children's Research Institute, Little Rock, AR, USA. REFrye@uams.edu.ORCID 0000-0003-4442-2937
Shannon RoseArkansas Children's Research Institute, Little Rock, AR, USA.ORCID 0000-0003-0595-4367
Rebecca WynneArkansas Children's Research Institute, Little Rock, AR, USA.
Sirish C BennuriArkansas Children's Research Institute, Little Rock, AR, USA.
Sarah BlossomArkansas Children's Research Institute, Little Rock, AR, USA.
Kathleen M GilbertArkansas Children's Research Institute, Little Rock, AR, USA.
Lynne HeilbrunDepartment of Family and Community Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
Raymond F PalmerDepartment of Family and Community Medicine, University of Texas Health Science Center, San Antonio, TX, USA.
Arkansas Children's Hospital · USThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitoplasticity occurs when mitochondria adapt to tolerate stressors. Previously we hypothesized that a subset of lymphoblastoid cell lines (LCLs) from children with autistic disorder (AD) show mitoplasticity (AD-A), presumably due to previous environmental exposures; another subset of AD LCLs demonstrated normal mitochondrial activity (AD-N). To better understand mitoplasticity in the AD-A LCLs we examined changes in mitochondrial function using the Seahorse XF96 analyzer in AD and Control LCLs after exposure to trichloroacetaldehyde hydrate (TCAH), an in vivo metabolite of the environmental toxicant and common environmental pollutant trichloroethylene. To better understand the role of reactive oxygen species (ROS) in mitoplasticity, TCAH exposure was followed by acute exposure to 2,3-dimethoxy-1,4-napthoquinone (DMNQ), an agent that increases ROS. TCAH exposure by itself resulted in a decline in mitochondrial respiration in all LCL groups. This effect was mitigated when TCAH was followed by acute DMNQ exposure but this varied across LCL groups. DMNQ did not affect AD-N LCLs, while it neutralized the detrimental effect of TCAH in Control LCLs and resulted in a increase in mitochondrial respiration in AD-A LCLs. These data suggest that acute increases in ROS can activate mitochondrial protective pathways and that AD-A LCLs are better able to activate these protective pathways.

Indexed as

Oxidative StressAdenosine TriphosphateAutistic DisorderCell LineCell RespirationChloral HydrateHumansLymphocytesMitochondriaOxidation-ReductionProtonsReactive Oxygen SpeciesAdenosine TriphosphateChloral HydrateProtonsReactive Oxygen Speciestrichloroacetaldehyde

Identifiers

PMID28667285
PMCPMC5493637
OpenAlexW2705551680

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.