Evidence map›Paper›PMID 22476699›Full record

ArticleNeurochemical research2012

Effects of selenium on calcium signaling and apoptosis in rat dorsal root ganglion neurons induced by oxidative stress.

Abdülhadi Cihangir Uğuz, Mustafa Nazıroğlu

Abstract read
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In one paragraph

Article in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
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  12. Neonatal Anesthesia and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022
    Review
  13. Review
  14. Selenium at theFrontiers in neuroscience · 2021
    Review
  15. Neuroprotective Effect of Antioxidants in the Brain.International journal of molecular sciences · 2020
    Review
  16. (Z)-7,4'-dimethoxy-6-hydroxy-aurone-4-O-The Journal of international medical research · 2020
    Article
  17. Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020
    Article
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Abdülhadi Cihangir UğuzDepartment of Biophysics, Faculty of Medicine, Süleyman Demirel University, Dekanlık Binasi, 32260 Isparta, Turkey.
Mustafa Nazıroğlu
Süleyman Demirel University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ca(2+) is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca(2+) overload is detrimental to cellular function and may present as an important cause of cellular oxidative stress generation and apoptosis. The aim of this study is to investigate the effects of selenium on lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), cytosolic Ca(2+) release, cell viability (MTT) and apoptosis values in dorsal root ganglion (DRG) sensory neurons of rats. DRG cells were divided into four groups namely control, H(2)O(2) (as a model substance used as a paradigm for oxidative stress), selenium, selenium + H(2)O(2). Moderate doses and times of H(2)O(2) and selenium were determined by MTT test. Cells were preterated 200 nM selenium for 30 h before incubatation with 1 μM H(2)O(2) for 2 h. Lipid peroxidation levels were lower in the control, selenium, selenium + H(2)O(2) groups than in the H(2)O(2) group. GSH-Px activities were higher in the selenium groups than in the H(2)O(2) group. GSH levels were higher in the control, selenium, selenium + H(2)O(2) groups than in the H(2)O(2) group. Cytosolic Ca(2+) release was higher in the H(2)O(2) group than in the control, selenium, selenium + H(2)O(2) groups. Cytosolic Ca(2+) release was lower in the selenium + H(2)O(2) group than in the H(2)O(2). In conclusion, the present study demonstrates that selenium induced protective effects on oxidative stress, [Ca(2+)](c) release and apoptosis in DRG cells. Since selenium deficiency is a common feature of oxidative stress-induced neurological diseases of sensory neurons, our findings are relevant to the etiology of pathology in oxidative stress-induced neurological diseases of the DRG neurons.

Indexed as

AnimalsApoptosisCalciumCalcium SignalingCytosolGanglia, SpinalGlutathioneGlutathione PeroxidaseHydrogen PeroxideLipid PeroxidationOxidative StressRatsRats, WistarSeleniumSensory Receptor CellsCalciumGlutathioneGlutathione PeroxidaseHydrogen PeroxideSelenium

Identifiers

PMID22476699
OpenAlexW1970796115

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.