Evidence map›Paper›PMID 27023069›Full record

ArticlePLoS neglected tropical diseases2016

Allicin Induces Calcium and Mitochondrial Dysregulation Causing Necrotic Death in Leishmania.

María J Corral, Elena Benito-Peña, M Dolores Jiménez-Antón, Laureano Cuevas, María C Moreno-Bondi, José M Alunda

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2016. 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
11.7field-weighted citation impact, top 2% 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, 54 citations in OpenAlex.

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  5. Novel Schiff bases of Vanillin: potent inhibitors of macrophage harboredJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2023
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  16. Activity of Thioallyl Compounds From Garlic AgainstFrontiers in cellular and infection microbiology · 2018
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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

6 authors at 2 institutions in 1 country.

María J CorralDepartment of Animal Health, Group ICPVet, Faculty of Veterinary Medicine, University Complutense Madrid, Spain.
Elena Benito-PeñaDepartment of Analytical Chemistry, Optical Chemosensors and Applied Photochemistry Group (GSOLFA), University Complutense Madrid, Spain.
M Dolores Jiménez-AntónDepartment of Animal Health, Group ICPVet, Faculty of Veterinary Medicine, University Complutense Madrid, Spain.
Laureano CuevasNational Microbiology Centre, Institute of Health Carlos III (ISCIII), Majadahonda, Madrid, Spain.
María C Moreno-BondiDepartment of Analytical Chemistry, Optical Chemosensors and Applied Photochemistry Group (GSOLFA), University Complutense Madrid, Spain.
José M AlundaDepartment of Animal Health, Group ICPVet, Faculty of Veterinary Medicine, University Complutense Madrid, Spain.
Universidad Complutense de Madrid · ESCentro Nacional de Sanidad Ambiental · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAllicin has shown antileishmanial activity in vitro and in vivo. However the mechanism of action underlying its antiproliferative effect against Leishmania has been virtually unexplored. In this paper, we present the results obtained in L.infantum and a mechanistic basis is proposed. METHODOLOGY/PRINCIPAL FINDING: Exposure of the parasites to allicin led to high Ca2+ levels and mitochondrial reactive oxygen species (ROS), collapse of the mitochondrial membrane potential, reduced production of ATP and elevation of cytosolic ROS. The incubation of the promastigotes with SYTOX Green revealed that decrease of ATP was not associated with plasma membrane permeabilization. Annexin V and propidium iodide (PI) staining indicated that allicin did not induce phospholipids exposure on the plasma membrane. Moreover, DNA agarose gel electrophoresis and TUNEL analysis demonstrated that allicin did not provoke DNA fragmentation. Analysis of the cell cycle with PI staining showed that allicin induced cell cycle arrest in the G2/M phase. CONCLUSIONS/SIGNIFICANCE: We conclude that allicin induces dysregulation of calcium homeostasis and oxidative stress, uncontrolled by the antioxidant defense of the cell, which leads to mitochondrial dysfunction and a bioenergetic catastrophe leading to cell necrosis and cell cycle arrest in the premitotic phase.

Indexed as

Adenosine TriphosphateApoptosisCalciumDisulfidesDose-Response Relationship, DrugLeishmaniaMembrane Potential, MitochondrialMitochondriaReactive Oxygen SpeciesSulfinic AcidsAdenosine TriphosphateallicinCalciumDisulfidesReactive Oxygen SpeciesSulfinic Acids

Identifiers

PMID27023069
PMCPMC4811430
OpenAlexW2318262213

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.