Evidence map›Paper›PMID 24969583›Full record

ArticleMolecular neurobiology2015

Melatonin inhibits manganese-induced motor dysfunction and neuronal loss in mice: involvement of oxidative stress and dopaminergic neurodegeneration.

Yu Deng, Congcong Jiao, Chao Mi, Bin Xu, Yuehui Li, Fei Wang, Wei Liu, Zhaofa Xu

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 12% 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, 46 citations in OpenAlex.

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  13. Melatonin and mitochondrial function during ischemia/reperfusion injury.Cellular and molecular life sciences : CMLS · 2017
    Review
  14. Review
  15. Redox dynamics of manganese as a mitochondrial life-death switch.Biochemical and biophysical research communications · 2017
    Review
  16. Article
  17. Article
  18. Review
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 2 institutions in 1 country.

Yu DengDepartment of Environmental Health, School of Public Health, China Medical University, North 2nd Road 92, Heping ward, Shenyang, Liaoning, 110001, People's Republic of China, dengyu.cmu@163.com.
Congcong Jiao
Chao Mi
Bin Xu
Yuehui Li
Fei Wang
Wei Liu
Zhaofa Xu
China Medical University · CNShenyang Institute of Engineering · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive manganese (Mn) induces oxidative stress and dopaminergic neurodegeneration. However, the relationship between them during Mn neurotoxicity has not been clarified. The purpose of this study was to investigate the probable role of melatonin (MLT) against Mn-induced motor dysfunction and neuronal loss as a result of antagonizing oxidative stress and dopaminergic neurodegeneration. Mice were randomly divided into five groups as follows: control, MnCl2, low MLT + MnCl2, median MLT + MnCl2, and high MLT + MnCl2. Administration of MnCl2 (50 mg/kg) for 2 weeks significantly induced hypokinesis, dopaminergic neurons degeneration and loss, neuronal ultrastructural damage, and apoptosis in the substantia nigra and the striatum. These conditions were caused in part by the overproduction of reactive oxygen species, malondialdehyde accumulation, and dysfunction of the nonenzymatic (GSH) and enzymatic (GSH-Px, superoxide dismutase, quinone oxidoreductase 1, glutathione S-transferase, and glutathione reductase) antioxidative defense systems. Mn-induced neuron degeneration, astrocytes, and microglia activation contribute to the changes of oxidative stress markers. Dopamine (DA) depletion and downregulation of DA transporter and receptors were also found after Mn administration, this might also trigger motor dysfunction and neurons loss. Pretreatment with MLT prevented Mn-induced oxidative stress and dopaminergic neurodegeneration and inhibited the interaction between them. As a result, pretreatment with MLT significantly alleviated Mn-induced motor dysfunction and neuronal loss. In conclusion, Mn treatment resulted in motor dysfunction and neuronal loss, possibly involving an interaction between oxidative stress and dopaminergic neurodegeneration in the substantia nigra and the striatum. Pretreatment with MLT attenuated Mn-induced neurotoxicity by means of its antioxidant properties and promotion of the DA system.

Indexed as

AnimalsAntioxidantsApoptosisCD11b AntigenChloridesDopamineDopamine Plasma Membrane Transport ProteinsDopaminergic NeuronsFemaleGlial Fibrillary Acidic ProteinGlutathioneImmunohistochemistryMaleMalondialdehydeManganese CompoundsMelatoninAntioxidantsCD11b AntigenChloridesDopamineDopamine Plasma Membrane Transport ProteinsGlial Fibrillary Acidic ProteinGlutathioneMalondialdehydemanganese chlorideManganese CompoundsMelatoninPhosphopyruvate HydrataseReactive Oxygen SpeciesReceptors, DopamineTyrosine 3-Monooxygenase

Identifiers

PMID24969583
OpenAlexW2169989061

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.