Evidence map›Paper›PMID 31034624›Full record

ArticleEnvironmental toxicology and chemistry2019

Linking Mitochondrial Dysfunction to Organismal and Population Health in the Context of Environmental Pollutants: Progress and Considerations for Mitochondrial Adverse Outcome Pathways.

David A Dreier, Danielle F Mello, Joel N Meyer, Christopher J Martyniuk

Open access · greenAbstract read
In one paragraph

Article in Environmental toxicology and chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
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  9. Review
  10. Environmental science & technology · 2022
    Article
  11. Rotenone ModulatesFrontiers in immunology · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Ecotoxico-lipidomics: An emerging concept to understand chemical-metabolic relationships in comparative fish models.Comparative biochemistry and physiology. Part D, Genomics & proteomics · 2020
    Review
  18. Article
  19. Article
  20. Arsenic Stimulates Myoblast Mitochondrial Epidermal Growth Factor Receptor to Impair Myogenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    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

4 authors at 2 institutions in 1 country.

David A DreierCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA.
Danielle F MelloNicholas School of the Environment, Duke University, Durham, North Carolina, USA.
Joel N MeyerNicholas School of the Environment, Duke University, Durham, North Carolina, USA.
Christopher J MartyniukCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA.
Duke University · USUniversity of Florida · US

Funding

Zebrafish as a Detector of Organophosphate ExposureP42ES010356 · NIEHS · DUKE UNIVERSITY · PI AMY H HERRING · 2000 to 2026
$56.2M
Does exposure to mitochondrial toxicants during germ cell development result in lifelong alterations in mitochondrial function mediated by epigenetic changes?R01ES028218 · NIEHS · DUKE UNIVERSITY · PI MEYER, JOEL NEWMAN · 2017 to 2021
$1.5M
NIEHS NIH HHS P42 ES010356NIEHS NIH HHS R01 ES028218NIH HHS P42ES010356 and R01ES028218NSF Cooperative Agreement EF-0830093NSF Graduate Research Fellowship Program DGE-1315138
6 · The paper itself

Abstract

Mitochondria are key targets of many environmental contaminants, because specific chemicals can interact directly with mitochondrial proteins, lipids, and ribonucleic acids. These direct interactions serve as molecular initiating events that impede adenosine triphosphate production and other critical functions that mitochondria serve within the cell (e.g., calcium and metal homeostasis, apoptosis, immune signaling, redox balance). A limited but growing number of adverse outcome pathways (AOPs) have been proposed to associate mitochondrial dysfunction with effects at organismal and population levels. These pathways involve key events such as altered membrane potential, mitochondrial fission/fusion, and mitochondrial DNA damage, among others. The present critical review and analysis reveals current progress on AOPs involving mitochondrial dysfunction, and, using a network-based computational approach, identifies the localization of mitochondrial molecular initiating events and key events within multiple existing AOPs. We also present 2 case studies, the first examining the interaction between mitochondria and immunotoxicity, and the second examining the role of early mitochondrial dysfunction in the context of behavior (i.e., locomotor activity). We discuss limitations in our current understanding of mitochondrial AOPs and highlight opportunities for clarifying their details. Advancing our knowledge of key event relationships within the AOP framework will require high-throughput datasets that permit the development and testing of chemical-agnostic AOPs, as well as high-resolution research that will enhance the mechanistic testing and validation of these key event relationships. Given the wide range of chemicals that affect mitochondria, and the centrality of energy production and signaling to ecologically important outcomes such as pathogen defense, homeostasis, growth, and reproduction, a better understanding of mitochondrial AOPs is expected to play a significant, if not central, role in environmental toxicology. Environ Toxicol Chem 2019;38:1625-1634. © 2019 SETAC.

Indexed as

Adverse Outcome PathwaysAnimalsEcotoxicologyEnvironmental PollutantsHumansMembrane Potential, MitochondrialMitochondriaMitochondrial DynamicsOxidation-ReductionPopulation HealthRisk AssessmentEnvironmental PollutantsAdverse outcome pathwaysHigh-throughput screeningImmune toxicityLocomotionMitochondriaWeight of evidence

Identifiers

PMID31034624
PMCPMC6961808
OpenAlexW2942870702

What OpenQuestion holds

Textmetadata
LicenceTDM
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.