Evidence map›Paper›PMID 28878165›Full record

ArticleInternational journal of molecular sciences2017

Mitochondrial Liver Toxicity of Valproic Acid and Its Acid Derivatives Is Related to Inhibition of α-Lipoamide Dehydrogenase.

Alexei P Kudin, Hafiz Mawasi, Arik Eisenkraft, Christian E Elger, Meir Bialer, Wolfram S Kunz

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  5. Review
  6. Review
  7. Article
  8. Article
  9. Factors Influencing Sodium Valproate Serum Concentrations in Patients with Epilepsy Based on Logistic Regression Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
  10. Article
  11. Review
  12. 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 2 institutions in 2 countries.

Alexei P KudinDepartment of Epileptology and Life & Brain Center, University of Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany. alexei_kudin@yahoo.com.
Hafiz MawasiInstitute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 91120, Israel. hmawasi@ekmd.huji.ac.il.
Arik EisenkraftInstitute for Research in Military Medicine, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 91120, Israel. arik@thoraxs.com.
Christian E ElgerDepartment of Epileptology and Life & Brain Center, University of Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany. christian.elger@ukbonn.de.
Meir BialerInstitute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 91120, Israel. meirb@ekmd.huji.ac.il.
Wolfram S KunzDepartment of Epileptology and Life & Brain Center, University of Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany. wolfram.kunz@ukbonn.de.ORCID 0000-0003-1113-3493
Hebrew University of Jerusalem · ILUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver toxicity of valproic acid (VPA) is an established side effect of this widely used antiepileptic drug, which is extremely problematic for patients with metabolic epilepsy and particularly epilepsy due to mitochondrial dysfunction. In the present report, we investigated the reason for liver mitochondrial toxicity of VPA and several acid and amide VPA analogues. While the pyruvate and 2-oxoglutarate oxidation rates of rat brain mitochondria were nearly unaffected by VPA, rat liver mitochondrial pyruvate and 2-oxoglutarate oxidation was severely impaired by VPA concentrations above 100 µM. Among the reactions involved in pyruvate oxidation, pyruvate transport and dehydrogenation steps were not affected by VPA, while α-lipoamide dehydrogenase was strongly inhibited. Strong inhibition of α-lipoamide dehydrogenase was also noted for the VPA one-carbon homolog

Indexed as

AmidesAnimalsDihydrolipoamide DehydrogenaseLiverMitochondriaMitochondria, LiverPyruvic AcidRatsValproic AcidAmidesDihydrolipoamide DehydrogenasePyruvic AcidvalnoctamideValproic Acidanalogues of valproic acidliver toxicitymetabolic epilepsymitochondrial epilepsyvalproic acid

Identifiers

PMID28878165
PMCPMC5618561
OpenAlexW2750703640

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.