Evidence map›Paper›PMID 25122772›Full record

ArticleThe Journal of biological chemistry2014

Inhibition of neuronal cell mitochondrial complex I with rotenone increases lipid β-oxidation, supporting acetyl-coenzyme A levels.

Andrew J Worth, Sankha S Basu, Nathaniel W Snyder, Clementina Mesaros, Ian A Blair

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  16. Autophagy and Redox Homeostasis in Parkinson's: A Crucial Balancing Act.Oxidative medicine and cellular longevity · 2020
    Review
  17. Mitochondrial NADAntioxidants & redox signaling · 2019
    Review
  18. Review
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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

5 authors at 1 institution in 1 country.

Andrew J WorthCenters for Cancer Pharmacology and Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160.
Sankha S BasuCenters for Cancer Pharmacology and Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160.
Nathaniel W SnyderCenters for Cancer Pharmacology and Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160.
Clementina MesarosCenters for Cancer Pharmacology and Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160.
Ian A BlairCenters for Cancer Pharmacology and Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160. Electronic address: ianblair@mail.med.upenn.edu.
University of Pennsylvania · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM008076 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BLENDY, JULIE A · 1985 to 2023
$10.8M
Translational Research Training Program in Environmental Health SciencesT32ES019851 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Kara A Bernstein, Trevor M Penning · 2012 to 2026
$6.0M
NIEHS NIH HHS P30 ES013508NIEHS NIH HHS P30ES013508NIEHS NIH HHS T32 ES019851NIEHS NIH HHS T32ES019851NIGMS NIH HHS T32 GM008076NIGMS NIH HHS T32GM008076
6 · The paper itself

Abstract

Rotenone is a naturally occurring mitochondrial complex I inhibitor with a known association with parkinsonian phenotypes in both human populations and rodent models. Despite these findings, a clear mechanistic link between rotenone exposure and neuronal damage remains to be determined. Here, we report alterations to lipid metabolism in SH-SY5Y neuroblastoma cells exposed to rotenone. The absolute levels of acetyl-CoA were found to be maintained despite a significant decrease in glucose-derived acetyl-CoA. Furthermore, palmitoyl-CoA levels were maintained, whereas the levels of many of the medium-chain acyl-CoA species were significantly reduced. Additionally, using isotopologue analysis, we found that β-oxidation of fatty acids with varying chain lengths helped maintain acetyl-CoA levels. Rotenone also induced increased glutamine utilization for lipogenesis, in part through reductive carboxylation, as has been found previously in other cell types. Finally, palmitoylcarnitine levels were increased in response to rotenone, indicating an increase in fatty acid import. Taken together, these findings show that alterations to lipid and glutamine metabolism play an important compensatory role in response to complex I inhibition by rotenone.

Indexed as

Acetyl Coenzyme ACell Line, TumorElectron Transport Complex IFatty AcidsGlutamineHumansNeuronsOxidation-ReductionPalmitoyl Coenzyme ARotenoneUncoupling AgentsAcetyl Coenzyme AElectron Transport Complex IFatty AcidsGlutaminePalmitoyl Coenzyme ARotenoneUncoupling AgentsAcetyl Coenzyme A (Acetyl-CoA)Cell MetabolismCoenzyme A (CoA)Complex IElectron TransportFatty Acid OxidationFatty Acid TransportLipidMass Spectrometry (MS)Neurodegenerative Disease

Identifiers

PMID25122772
PMCPMC4175330
OpenAlexW1994044009

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.