Evidence map›Paper›PMID 26418626›Full record

ArticleRedox biology2015

Ellagic acid, a polyphenolic compound, selectively induces ROS-mediated apoptosis in cancerous B-lymphocytes of CLL patients by directly targeting mitochondria.

Ahmad Salimi, Mehryar Habibi Roudkenar, Leila Sadeghi, Alireza Mohseni, Enayatollah Seydi, Nahal Pirahmadi, Jalal Pourahmad

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

40 citing papers in PubMed, 102 citations in OpenAlex.

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  15. TPEN exerts selective anti-leukemic efficacy in ex vivo drug-resistant childhood acute leukemia.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021
    Article
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  19. Review
  20. Induction of Apoptosis by Extract of Persian Gulf Marine Mollusk,Iranian journal of pharmaceutical research : IJPR · 2019
    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

7 authors at 3 institutions in 1 country.

Ahmad SalimiFaculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mehryar Habibi RoudkenarIranian Blood Transfusion Organization, Tehran, Iran.
Leila SadeghiShohadaye Tajrish Educational Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Alireza MohseniIranian Blood Transfusion Organization, Tehran, Iran.
Enayatollah SeydiFaculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Nahal PirahmadiFaculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Department of Pharmacology, Shiraz University, Shiraz, Iran.
Jalal PourahmadFaculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: j.pourahmadjaktaji@utoronto.ca.
Shahid Beheshti University of Medical Sciences · IRIranian Legal Medicine Organization · IRShiraz University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the effects ofellagic acid (EA) on the cytotoxicity, B-lymphocytes isolated from CLL patients and healthy individuals. Flow cytometric assay was used to measure the percentage of apoptosis versus necrosis, intracellular active oxygen radicals (ROS), mitochondrial membrane potential (MMP) and the caspase-3 activity and then mitochondria were isolated from both groups B-lymphocytes and parameters of mitochondrial toxicity was investigated. Based on our results EA decreased the percentage of viable cells and induced apoptosis. EA increased ROS formation, mitochondria swelling, MMP decrease and cytochrome c release in mitochondria isolated from CLL BUT NOT healthy B-lymphocytes while pre-treatment with cyclosporine A and Butylated hydroxyl toluene (BHT) prevented these effects. Our results suggest that EA can act as an anti cancer candidate by directly and selectively targeting mitochondria could induce apoptosis through mitochondria pathway with increasing ROS production which finally ends in cytochrome c release, caspase 3 activation and apoptosis in cancerous B-lymphocytes isolated from CLL patients.

Indexed as

ApoptosisAntineoplastic AgentsB-LymphocytesCaspase 3Cell SurvivalCytochromes cDrug Screening Assays, AntitumorEllagic AcidHumansLeukemia, Lymphocytic, Chronic, B-CellMembrane Potential, MitochondrialMitochondriaMitochondrial SwellingReactive Oxygen SpeciesAntineoplastic AgentsCASP3 protein, humanCaspase 3Cytochromes cEllagic AcidReactive Oxygen SpeciesActive oxygen radicals (ROS)ApoptosisChronic lymphocytic leukemia (CLL)Ellagic acidMitochondria

Identifiers

PMID26418626
PMCPMC4588415
OpenAlexW2214870473

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.