Evidence map›Paper›PMID 23629515›Full record

ReviewToxicological sciences : an official journal of the Society of Toxicology2013

Mitochondria as a target of environmental toxicants.

Joel N Meyer, Maxwell C K Leung, John P Rooney, Ataman Sendoel, Michael O Hengartner, Glen E Kisby, Amanda S Bess

Open access · bronzeAbstract readReview
In one paragraph

Review in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed
15.1field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 551 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Mitochondrial DNA Breaks and Copy Number and the Risk of Lung Cancer in the Shanghai Women's Health Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Progeny effects of rotenone exposure depend on parental toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  12. Article
  13. Chronic exposure to low levels of glyphosate and metals induces kidney dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

158 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 3 institutions in 2 countries.

Joel N MeyerNicholas School of the Environment, Duke University, Durham, NC, USA. joel.meyer@duke.edu
Maxwell C K Leung
John P Rooney
Ataman Sendoel
Michael O Hengartner
Glen E Kisby
Amanda S Bess
Duke University · USUniversity of Zurich · CHWestern University of Health Sciences · US

Funding

Zebrafish as a Detector of Organophosphate ExposureP42ES010356 · NIEHS · DUKE UNIVERSITY · PI AMY H HERRING · 2000 to 2026
$56.2M
The Role of Mitochondrial DNA Damage in NeurodegenerationR01ES017540 · NIEHS · DUKE UNIVERSITY · PI MEYER, JOEL NEWMAN · 2011 to 2015
$1.8M
NIEHS NIH HHS 1R01-ES017540-01A2NIEHS NIH HHS P42 ES010356NIEHS NIH HHS P42 ES010356-10A2NIEHS NIH HHS R01 ES017540
6 · The paper itself

Abstract

Enormous strides have recently been made in our understanding of the biology and pathobiology of mitochondria. Many diseases have been identified as caused by mitochondrial dysfunction, and many pharmaceuticals have been identified as previously unrecognized mitochondrial toxicants. A much smaller but growing literature indicates that mitochondria are also targeted by environmental pollutants. We briefly review the importance of mitochondrial function and maintenance for health based on the genetics of mitochondrial diseases and the toxicities resulting from pharmaceutical exposure. We then discuss how the principles of mitochondrial vulnerability illustrated by those fields might apply to environmental contaminants, with particular attention to factors that may modulate vulnerability including genetic differences, epigenetic interactions, tissue characteristics, and developmental stage. Finally, we review the literature related to environmental mitochondrial toxicants, with a particular focus on those toxicants that target mitochondrial DNA. We conclude that the fields of environmental toxicology and environmental health should focus more strongly on mitochondria.

Indexed as

DNA DamageDNA, MitochondrialAnimalsEnvironmental PollutantsHumansMitochondriaMitochondrial DiseasesMutagensDNA, MitochondrialEnvironmental PollutantsMutagenscontaminantsmitochondriamitochondrial disease.mitochondrial DNAmitochondrial toxicity

Identifiers

PMID23629515
PMCPMC3693132
OpenAlexW2103562463

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.