Evidence map›Paper›PMID 25688267›Full record

ArticleJournal of toxicology2015

Increased susceptibility to ethylmercury-induced mitochondrial dysfunction in a subset of autism lymphoblastoid cell lines.

Shannon Rose, Rebecca Wynne, Richard E Frye, Stepan Melnyk, S Jill James

Open access · goldAbstract read
In one paragraph

Article in Journal of toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 46 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

5 authors at 1 institution in 1 country.

Shannon RoseDepartment of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, 13 Children's Way, Slot 512-41B, Little Rock, AR 72202, USA.ORCID 0000-0003-0595-4367
Rebecca WynneDepartment of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, 13 Children's Way, Slot 512-41B, Little Rock, AR 72202, USA.
Richard E FryeDepartment of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, 13 Children's Way, Slot 512-41B, Little Rock, AR 72202, USA.
Stepan MelnykDepartment of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, 13 Children's Way, Slot 512-41B, Little Rock, AR 72202, USA.
S Jill JamesDepartment of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, 13 Children's Way, Slot 512-41B, Little Rock, AR 72202, USA.
Arkansas Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The association of autism spectrum disorders with oxidative stress, redox imbalance, and mitochondrial dysfunction has become increasingly recognized. In this study, extracellular flux analysis was used to compare mitochondrial respiration in lymphoblastoid cell lines (LCLs) from individuals with autism and unaffected controls exposed to ethylmercury, an environmental toxin known to deplete glutathione and induce oxidative stress and mitochondrial dysfunction. We also tested whether pretreating the autism LCLs with N-acetyl cysteine (NAC) to increase glutathione concentrations conferred protection from ethylmercury. Examination of 16 autism/control LCL pairs revealed that a subgroup (31%) of autism LCLs exhibited a greater reduction in ATP-linked respiration, maximal respiratory capacity, and reserve capacity when exposed to ethylmercury, compared to control LCLs. These respiratory parameters were significantly elevated at baseline in the ethylmercury-sensitive autism subgroup as compared to control LCLs. NAC pretreatment of the sensitive subgroup reduced (normalized) baseline respiratory parameters and blunted the exaggerated ethylmercury-induced reserve capacity depletion. These findings suggest that the epidemiological link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.

Identifiers

PMID25688267
PMCPMC4320799
OpenAlexW2055091062

What OpenQuestion holds

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LicenceCC BY
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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.