Evidence map›Paper›PMID 21799050›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2011

Effects of chlorpyrifos and chlorpyrifos-oxon on the dynamics and movement of mitochondria in rat cortical neurons.

Mary-Louise Middlemore-Risher, Bao-Ling Adam, Nevin A Lambert, Alvin V Terry

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.9field-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

40 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Article
  3. Chlorpyrifos and Chlorpyrifos-Oxon: A Widening Spectrum of Toxicity.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Is Gulf War Illness a prolonged early phase tauopathy?Cytoskeleton (Hoboken, N.J.) · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Use of computational toxicology tools to predictCurrent research in toxicology · 2022
    Article
  12. Article
  13. A cellular approach to understanding and treating Gulf War Illness.Cellular and molecular life sciences : CMLS · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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 2 countries.

Mary-Louise Middlemore-RisherProgram in Clinical and Experimental Therapeutics, University of Georgia, College of Pharmacy, Augusta, Georgia 30912-2450, USA.
Bao-Ling Adam
Nevin A Lambert
Alvin V Terry
Institute of Pharmacology · CZPhysiological Society · GB

Funding

Cholinesterase Inhibitors, Axonal Transport, and MemoryR01ES012241 · NIEHS · UNIVERSITY OF GEORGIA (UGA) · PI TERRY, ALVIN V · 2004 to 2013
$2.8M
NIEHS NIH HHS ES012241NIEHS NIH HHS R01 ES012241
6 · The paper itself

Abstract

Organophosphate (OP)-based pesticides have been used extensively for decades, and as a result, they have become almost ubiquitous in our environment. There is clinical and animal evidence to suggest that chronic exposures to OPs can lead to cognitive dysfunction and other neurological abnormalities, although the mechanism for these effects is unknown. We previously reported that repeated, subthreshold exposures (defined as doses not associated with signs of acute toxicity) to the commonly used OP chlorpyrifos (CPF) resulted in protracted impairments in the performance of attention and memory-related tasks in rodents as well as deficits in axonal transport ex vivo (in the sciatic nerve). Here, we investigated the effects of CPF and its active metabolite CPF oxon (CPO) on the dynamics and movement of mitochondria in rat primary cortical neurons using time-lapse imaging techniques. Exposure to CPF (1.0-20.0 μM) or CPO (5.0 nM-20.0 μM) for 1 or 24 h resulted in a concentration-dependent increase in mitochondrial length, a decrease in mitochondrial number (indicative of increased fusion events), and a decrease in their movement in axons. The changes occurred at concentrations of CPF and CPO that did not inhibit acetylcholinesterase activity (the commonly cited mechanism of acute OP toxicity), and they were not blocked by cholinergic receptor antagonists. Furthermore, the changes did not seem to be associated with direct (OP-related) effects on mitochondrial viability or function (i.e., mitochondrial membrane potential or ATP production). The results suggest that an underlying mechanism of organophosphate-based deficits in cognitive function might involve alterations in mitochondrial dynamics and/or their transport in axons.

Indexed as

AcetylcholinesteraseAdenosine TriphosphateAnimalsAxonal TransportAxonsCell MovementCerebral CortexChlorpyrifosCholinesterase InhibitorsDose-Response Relationship, DrugGPI-Linked ProteinsInsecticidesMembrane Potential, MitochondrialMitochondriaNeuronsNicotinic AntagonistsAcetylcholinesteraseAche protein, ratAdenosine TriphosphateChlorpyrifosCholinesterase InhibitorsGPI-Linked ProteinsInsecticidesNicotinic AntagonistsReceptors, CholinergicSuperoxides

Identifiers

PMID21799050
PMCPMC3199992
OpenAlexW2109519777

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.