Evidence map›Paper›PMID 19969594›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2010

Comparative cytotoxicity and intracellular accumulation of five polybrominated diphenyl ether congeners in mouse cerebellar granule neurons.

Suping C Huang, Gennaro Giordano, Lucio G Costa

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-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

33 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Polybrominated diphenyl ethers in the environment: a wake-up call for concerted action in India.Environmental science and pollution research international · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Co-Culture of Neurons and Microglia.Current protocols in toxicology · 2017
    Article
  16. Organ-on-a-chip for assessing environmental toxicants.Current opinion in biotechnology · 2017
    Review
  17. Autism, Mitochondria and Polybrominated Diphenyl Ether Exposure.CNS & neurological disorders drug targets · 2016
    Review
  18. A perspective on the potential risks of emerging contaminants to human and environmental health.Environmental science and pollution research international · 2015
    Review
  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 2 institutions in 2 countries.

Suping C HuangDepartment of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington 98105, USA.
Gennaro Giordano
Lucio G Costa
University of Washington · USUniversity of Washington Applied Physics Laboratory · US

Funding

XENOBIOTIC BIOTRANSFORMATION AND DISPOSITIONP30ES007033 · NIEHS · UNIVERSITY OF WASHINGTON · PI ALI SHOJAIE · 1995 to 2026
$42.5M
NIEHS NIH HHS P30 ES007033NIEHS NIH HHS P30ES07033
6 · The paper itself

Abstract

Polybrominated diphenyl ethers (PBDEs), a group of flame retardants comprising 209 congeners, have become widespread environmental pollutants. High levels of PBDEs have been detected in human tissues, particularly in North America, and body burden is especially high in infants and toddlers because of exposure through breast milk and house dust. Increasing evidence, provided by animal studies, suggests that PBDEs are developmental neurotoxicants, although the underlying mechanisms are still unknown. Various PBDEs have been reported to cause oxidative stress and to induce apoptotic cell death in several cell types. In the present study, we investigated the comparative neurotoxicity in mouse cerebellar granule neurons of five brominated diphenyl ether (BDE) congeners, chosen among the most commonly found at the highest levels in human tissues. All BDE congener tested (BDE-47, BDE-99, BDE-100, BDE-153, and BDE-209) decreased cell viability and induced apoptotic cell death, which was prevented by antioxidants. They also caused oxidative stress, as indicated by an increase in reactive oxygen species and in lipid peroxidation. For all end points measured, the potency ranking of the congeners was BDE-100 > BDE-47 > BDE-99 > BDE-153 >> BDE-209. Measurement of BDE congener levels in neurons after exposure to different concentrations showed a significant accumulation in cells, which followed the same relative ranking. The findings suggest that all BDE congeners tested exhibit the same general mode of action (induction of oxidative stress-mediated apoptosis) and that the ability of each isomer to elicit such effects is dependent upon their accumulation in neurons, particularly in the microsomal fraction and the mitochondria.

Indexed as

AnimalsCells, CulturedCell SurvivalCerebellumFlame RetardantsHalogenated Diphenyl EthersMiceNeuronsOxidative StressToxicity TestsFlame RetardantsHalogenated Diphenyl Ethers

Identifiers

PMID19969594
PMCPMC2819972
OpenAlexW2104992683

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.