Evidence map›Paper›PMID 23347615›Full record

ArticleMolecular autism2013

Evidence of reactive oxygen species-mediated damage to mitochondrial DNA in children with typical autism.

Eleonora Napoli, Sarah Wong, Cecilia Giulivi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular autism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
8.3field-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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Ubiquinol improves symptoms in children with autism.Oxidative medicine and cellular longevity · 2014
    Trial
  3. Review
  4. Review
  5. A Developmental Neuroimmune Cascade Model of Autism Spectrum Disorder.International journal of molecular sciences · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Signaling pathways in hair aging.Frontiers in cell and developmental biology · 2023
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Eleonora NapoliDepartment of Molecular Biosciences, University of California, One Shields Ave, 1120 Haring Hall, Davis, CA, 95616, USA. cgiulivi@ucdavis.edu.
Sarah Wong
Cecilia Giulivi
University of California, Davis · US

Funding

THE CHARGE STUDY: CHILDHOOD AUTISM RISKS FROM GENETICS AND THE ENVIRONMENT - ADMINISTRATIVE SUPPLEMENTR01ES015359 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HERTZ-PICCIOTTO, IRVA · 2007 to 2019
$13.8M
Electron Paramagnetic Resonance SpectrometerS10RR023586 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GIULIVI, CECILIA · 2009 to 2009
$475k
Antioxidants and oxidative damage in mitochondriaR01ES012691 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI GIULIVI, CECILIA · 2004 to 2004
$148k
NIEHS NIH HHS R01 ES015359
6 · The paper itself

Abstract

unlabelled

backgroundThe mitochondrial genome (mtDNA) is particularly susceptible to damage mediated by reactive oxygen species (ROS). Although elevated ROS production and elevated biomarkers of oxidative stress have been found in tissues from children with autism spectrum disorders, evidence for damage to mtDNA is lacking.

findingsmtDNA deletions were evaluated in peripheral blood monocytic cells (PBMC) isolated from 2-5 year old children with full autism (AU; n = 67), and typically developing children (TD; n = 46) and their parents enrolled in the CHildhood Autism Risk from Genes and Environment study (CHARGE) at University of California Davis. Sequence variants were evaluated in mtDNA segments from AU and TD children (n = 10; each) and their mothers representing 31.2% coverage of the entire human mitochondrial genome. Increased mtDNA damage in AU children was evidenced by (i) higher frequency of mtDNA deletions (2-fold), (ii) higher number of GC→AT transitions (2.4-fold), being GC preferred sites for oxidative damage, and (iii) higher frequency of G,C,T→A transitions (1.6-fold) suggesting a higher incidence of polymerase gamma incorporating mainly A at bypassed apurinic/apyrimidinic sites, probably originated from oxidative stress. The last two outcomes were identical to their mothers suggesting the inheritance of a template consistent with increased oxidative damage, whereas the frequency of mtDNA deletions in AU children was similar to that of their fathers.

conclusionsThese results suggest that a combination of genetic and epigenetic factors, taking place during perinatal periods, results in a mtDNA template in children with autism similar to that expected for older individuals.

Identifiers

PMID23347615
PMCPMC3570390
OpenAlexW2152240719

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.