Evidence map›Paper›PMID 19307255›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism.

S Jill James, Shannon Rose, Stepan Melnyk, Stefanie Jernigan, Sarah Blossom, Oleksandra Pavliv, David W Gaylor

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 2% 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

113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Sulforaphane treatment of autism spectrum disorder (ASD).Proceedings of the National Academy of Sciences of the United States of America · 2014
    Trial
  5. Trial
  6. Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium-glutathione axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
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  16. Brain glutathione and GABA+ levels in autistic children.Autism research : official journal of the International Society for Autism Research · 2024
    Article
  17. Article
  18. Review
  19. Review
  20. Article

53 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

S Jill JamesDepartment of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, 1120 Marshall St., Little Rock, AR 72202, USA. jamesjill@uams.edu
Shannon Rose
Stepan Melnyk
Stefanie Jernigan
Sarah Blossom
Oleksandra Pavliv
David W Gaylor
University of Arkansas for Medical Sciences · USArkansas Children's Hospital · US

Funding

Metabolic Biomarkers of Autism: Predictive Potential and Genetic SusceptibilityR01HD051873 · NICHD · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI JAMES, SANDRA JILL · 2006 to 2010
$1.8M
NICHD NIH HHS R01 HD051873
6 · The paper itself

Abstract

Research into the metabolic phenotype of autism has been relatively unexplored despite the fact that metabolic abnormalities have been implicated in the pathophysiology of several other neurobehavioral disorders. Plasma biomarkers of oxidative stress have been reported in autistic children; however, intracellular redox status has not yet been evaluated. Lymphoblastoid cells (LCLs) derived from autistic children and unaffected controls were used to assess relative concentrations of reduced glutathione (GSH) and oxidized disulfide glutathione (GSSG) in cell extracts and isolated mitochondria as a measure of intracellular redox capacity. The results indicated that the GSH/GSSG redox ratio was decreased and percentage oxidized glutathione increased in both cytosol and mitochondria in the autism LCLs. Exposure to oxidative stress via the sulfhydryl reagent thimerosal resulted in a greater decrease in the GSH/GSSG ratio and increase in free radical generation in autism compared to control cells. Acute exposure to physiological levels of nitric oxide decreased mitochondrial membrane potential to a greater extent in the autism LCLs, although GSH/GSSG and ATP concentrations were similarly decreased in both cell lines. These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromise antioxidant defense and detoxification capacity under prooxidant conditions.

Indexed as

Adenosine TriphosphateAdolescentAdultAutistic DisorderCase-Control StudiesCell LineChildCytosolFree RadicalsGlutathioneGlutathione DisulfideHumansLymphocytesMaleMembrane Potential, MitochondrialMitochondriaAdenosine TriphosphateFree RadicalsGlutathioneGlutathione DisulfideS-Nitroso-N-AcetylpenicillamineThimerosal

Identifiers

PMID19307255
PMCPMC2717775
OpenAlexW2139174791

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.