Evidence map›Paper›PMID 29069497›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2018

From the Cover: Harmane-Induced Selective Dopaminergic Neurotoxicity in Caenorhabditis elegans.

Shreesh Raj Sammi, Zeynep Sena Agim, Jason R Cannon

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  3. Review
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  9. Article
  10. Article
  11. Review
  12. Frontiers in toxicology · 2022
    Article
  13. Neurotoxicity and Underlying Mechanisms of Endogenous Neurotoxins.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Xenobiotic metabolism and transport inJournal of toxicology and environmental health. Part B, Critical reviews · 2021
    Review
  16. Article
  17. Modeling Parkinson's Disease: Not Only Rodents?Frontiers in aging neuroscience · 2021
    Article
  18. Article
  19. Article
  20. Neuromelanin Modulates Heterocyclic Aromatic Amine-Induced Dopaminergic Neurotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    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

3 authors at 1 institution in 1 country.

Shreesh Raj SammiSchool of Health Sciences.
Zeynep Sena AgimSchool of Health Sciences.
Jason R CannonSchool of Health Sciences.
Purdue University West Lafayette · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Mechanisms of PhIP-induced dopaminergic neurotoxicityR01ES025750 · NIEHS · PURDUE UNIVERSITY · PI Jason R Cannon · 2016 to 2026
$4.2M
NIEHS NIH HHS R01 ES025750NIH HHS P40 OD010440
6 · The paper itself

Abstract

Parkinson's disease (PD) is a debilitating neurodegenerative disease. Although numerous exposures have been linked to PD etiology, causative factors for most cases remain largely unknown. Emerging data on the neurotoxicity of heterocyclic amines suggest that this class of compounds should be examined for relevance to PD. Here, using Caenorhabditis elegans as a model system, we tested whether harmane exposure produced selective toxicity to dopamine neurons that is potentially relevant to PD. Harmane is a known tremorigenic β-carboline (a type of heterocyclic amine) found in cooked meat, roasted coffee beans, and tobacco. Thus, this compound represents a potentially important exposure. In the nematode model, we observed dopaminergic neurons to be selectively vulnerable, showing significant loss in terms of structure and function at lower doses than other neuronal populations. In examining mechanisms of toxicity, we observed significant harmane-induced decreases in mitochondrial viability and increased reactive oxygen species levels. Blocking transport through the dopamine transporter (DAT) was not neuroprotective, suggesting that harmane is unlikely to enter the cell through DAT. However, a mitochondrial complex I activator did partially ameliorate neurodegeneration. Further, mitochondrial complex I activator treatment reduced harmane-induced dopamine depletion, measured by the 1-nonanol assay. In summary, we have shown that harmane exposure in C. elegans produces selective dopaminergic neurotoxicity that may bear relevance to PD, and that neurotoxicity may be mediated through mitochondrial mechanisms.

Indexed as

AnimalsCaenorhabditis elegansDietary ExposureDisease Models, AnimalDopaminergic NeuronsHarmineMitochondriaParkinson Disease, SecondaryReactive Oxygen SpeciesharmanHarmineReactive Oxygen SpeciesC.elegansdopamineharmaneneurodegenerationParkinson’s disease

Identifiers

PMID29069497
PMCPMC5837500
OpenAlexW2767019639

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.