Evidence map›Paper›PMID 26462443›Full record

ArticleScientific reports2015

Mitochondrial respiratory dysfunction due to the conversion of substituted cathinones to methylbenzamides in SH-SY5Y cells.

Bjørnar den Hollander, Mira Sundström, Anna Pelander, Antti Siltanen, Ilkka Ojanperä, Eero Mervaala, Esa R Korpi, Esko Kankuri

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. 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
2.6field-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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. 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

8 authors at 1 institution in 1 country.

Bjørnar den HollanderDepartment of Pharmacology, Faculty of Medicine, Biomedicum Helsinki, Haartmaninkatu 8, FI-00014 University of Helsinki, Finland.
Mira SundströmDepartment of Forensic Medicine, Kytösuontie 11, FI-00014 University of Helsinki, Finland.
Anna PelanderDepartment of Forensic Medicine, Kytösuontie 11, FI-00014 University of Helsinki, Finland.
Antti SiltanenDepartment of Pharmacology, Faculty of Medicine, Biomedicum Helsinki, Haartmaninkatu 8, FI-00014 University of Helsinki, Finland.
Ilkka OjanperäDepartment of Forensic Medicine, Kytösuontie 11, FI-00014 University of Helsinki, Finland.
Eero MervaalaDepartment of Pharmacology, Faculty of Medicine, Biomedicum Helsinki, Haartmaninkatu 8, FI-00014 University of Helsinki, Finland.
Esa R KorpiDepartment of Pharmacology, Faculty of Medicine, Biomedicum Helsinki, Haartmaninkatu 8, FI-00014 University of Helsinki, Finland.
Esko KankuriDepartment of Pharmacology, Faculty of Medicine, Biomedicum Helsinki, Haartmaninkatu 8, FI-00014 University of Helsinki, Finland.
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increased use of cathinone-type designer drugs, known as legal highs, has led to concerns about their potential neurotoxicity due to their similarity to methamphetamine (METH). Therefore, closer investigations of their toxic effects are needed. We investigated the effects of the cathinones 4-methylmethcathinone (4-MMC) and 3,4-methylenedioxymethcathinone (MDMC) and the amphetamine METH on cytotoxicity and mitochondrial respiration in SH-SY5Y neuroblastoma cells. We also investigated the contribution of reactive species, dopamine, Bcl-2 and tumor necrosis factor α (TNFα) on toxicity. Finally, we investigated the effect of cathinone breakdown products using ultra-high performance liquid chromatography/high-resolution time-of-flight mass spectrometry and studied their involvement in toxicity. We observed dose-dependent increases in cytotoxicity and decreases in mitochondrial respiration following treatment with all cathinones and amphetamines. Glutathione depletion increases amphetamine, but not cathinone toxicity. Bcl-2 and TNFα pathways are involved in toxicity but dopamine levels are not. We also show that cathinones, but not amphetamines, spontaneously produce reactive species and cytotoxic methylbenzamide breakdown products when in aqueous solution. These results provide an important first insight into the mechanisms of cathinone cytotoxicity and pave the way for further studies on cathinone toxicity in vivo.

Indexed as

AlkaloidsBenzamidesCell LineCell SurvivalDose-Response Relationship, DrugHumansMethylationMitochondriaMitochondrial DiseasesNeuronsAlkaloidsBenzamidescathinone

Identifiers

PMID26462443
PMCPMC4604489
OpenAlexW2408316768

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.