Evidence map›Paper›PMID 34226525›Full record

ArticleCell death discovery2021

Impairment of neuronal mitochondrial function by L-DOPA in the absence of oxygen-dependent auto-oxidation and oxidative cell damage.

Philipp Hörmann, Sylvie Delcambre, Jasmin Hanke, Robert Geffers, Marcel Leist, Karsten Hiller

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Catechol-Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Levodopa-induced dyskinesia: brain iron deposition as a new hypothesis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. DOPA Homeostasis by Dopamine: A Control-Theoretic View.International journal of molecular sciences · 2021
    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

6 authors at 4 institutions in 2 countries.

Philipp HörmannDepartment of Bioinformatics and Biochemistry, Technische Universität Braunschweig, Braunschweig, Germany.
Sylvie DelcambreLuxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
Jasmin HankeDepartment of Bioinformatics and Biochemistry, Technische Universität Braunschweig, Braunschweig, Germany.
Robert GeffersGenome Analytics, Helmholtz-Center for Infection Research, Braunschweig, Germany.ORCID http://orcid.org/0000-0003-4409-016X
Marcel LeistIn Vitro Toxicology and Biomedicine, University of Konstanz, Konstanz, Germany.ORCID http://orcid.org/0000-0002-3778-8693
Karsten HillerDepartment of Bioinformatics and Biochemistry, Technische Universität Braunschweig, Braunschweig, Germany. karsten.hiller@tu-braunschweig.de.
Technische Universität Braunschweig · DEHelmholtz Centre for Infection Research · DEUniversity of Konstanz · DEUniversity of Luxembourg · LU

Funding

Fonds National de la Recherche Luxembourg (National Research Fund) CORE THActivity
6 · The paper itself

Abstract

L-3,4-Dihydroxyphenylalanin (L-DOPA or levodopa) is currently the most used drug to treat symptoms of Parkinson's disease (PD). After crossing the blood-brain barrier, it is enzymatically converted to dopamine by neuronal cells and restores depleted endogenous neurotransmitter levels. L-DOPA is prone to auto-oxidation and reactive intermediates of its degradation including reactive oxygen species (ROS) have been implicated in cellular damage. In this study, we investigated how oxygen tension effects L-DOPA stability. We applied oxygen tensions comparable to those in the mammalian brain and demonstrated that 2% oxygen almost completely stopped its auto-oxidation. L-DOPA even exerted a ROS scavenging function. Further mechanistic analysis indicated that L-DOPA reprogrammed mitochondrial metabolism and reduced oxidative phosphorylation, depolarized the mitochondrial membrane, induced reductive glutamine metabolism, and depleted the NADH pool. These results shed new light on the cellular effects of L-DOPA and its neuro-toxicity under physiological oxygen levels that are very distinct to normoxic in vitro conditions.

Identifiers

PMID34226525
PMCPMC8257685
OpenAlexW3181155932

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.