Evidence map›Paper›PMID 27861548›Full record

ArticlePloS one2016

Targeting Mitochondrial Dysfunction with L-Alpha Glycerylphosphorylcholine.

Gerda Strifler, Eszter Tuboly, Anikó Görbe, Mihály Boros, Daniella Pécz, Petra Hartmann

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
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  7. Choline supplements: An update.Frontiers in endocrinology · 2023
    Review
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  11. Observational
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  14. Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Article
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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

6 authors at 1 institution in 1 country.

Gerda StriflerInstitute of Surgical Research, University of Szeged, Szeged, Hungary.
Eszter TubolyInstitute of Surgical Research, University of Szeged, Szeged, Hungary.
Anikó GörbeDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
Mihály BorosInstitute of Surgical Research, University of Szeged, Szeged, Hungary.
Daniella PéczInstitute of Surgical Research, University of Szeged, Szeged, Hungary.
Petra HartmannInstitute of Surgical Research, University of Szeged, Szeged, Hungary.
University of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe hypothesized that L-alpha-glycerylphosphorylcholine (GPC), a deacylatedphosphatidylcholine derivative, can influence the mitochondrial respiratory activity and in this way, may exert tissue protective effects.

methodsRat liver mitochondria were examined with high-resolution respirometry to analyze the effects of GPC on the electron transport chain in normoxic and anoxic conditions. Besides, Sprague-Dawley rats were subjected to sham operation or standardized liver ischemia-reperfusion (IR), with or without GPC administration. The reduced glutathione (GSH) and oxidized glutathione disulfide (GSSG), the tissue myeloperoxidase, xanthine oxidoreductase and NADPH oxidases activities were measured. Tissue malondialdehyde and nitrite/nitrate formation, together with blood superoxide and hydrogen-peroxide production were assessed.

resultsGPC increased the efficacy of complex I-linked mitochondrial oxygen consumption, with significantly lower in vitro leak respiration. Mechanistically, liver IR injury was accompanied by deteriorated mitochondrial respiration and enhanced ROS production and, as a consequence, by significantly increased inflammatory enzyme activities. GPC administration decreased the inflammatory activation in line with the reduced oxidative and nitrosative stress markers.

conclusionGPC, by preserving the mitochondrial complex I function respiration, reduced the biochemical signs of oxidative stress after an IR episode. This suggests that GPC is a mitochondria-targeted compound that indirectly suppresses the activity of major intracellular superoxide-generating enzymes.

Indexed as

AnimalsGlutathioneGlutathione DisulfideGlycerylphosphorylcholineLiverMaleMalondialdehydeMitochondriaMitochondria, LiverNADPH OxidasesNitric OxideOxidation-ReductionOxidative StressOxygen ConsumptionRatsReperfusion InjuryGlutathioneGlutathione DisulfideGlycerylphosphorylcholineMalondialdehydeNADPH OxidasesNitric OxideXanthine Dehydrogenase

Identifiers

PMID27861548
PMCPMC5115775
OpenAlexW2549748085

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.