Evidence map›Paper›PMID 24667842›Full record

ArticlePloS one2014

Sulforaphane induces oxidative stress and death by p53-independent mechanism: implication of impaired glutathione recycling.

José Miguel P Ferreira de Oliveira, Maria Costa, Tiago Pedrosa, Pedro Pinto, Catarina Remédios, Helena Oliveira, Francisco Pimentel, Luís Almeida, Conceição Santos

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
2.8field-weighted citation impact, top 9% 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.

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  16. Sulforaphane Modulates AQP8-Linked Redox Signalling in Leukemia Cells.Oxidative medicine and cellular longevity · 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

9 authors at 3 institutions in 1 country.

José Miguel P Ferreira de OliveiraCESAM & Laboratory of Biotechnology and Cytomics, Department of Biology, University of Aveiro, Campus Universitário de Santiago, Aveiro, Portugal.
Maria CostaCESAM & Laboratory of Biotechnology and Cytomics, Department of Biology, University of Aveiro, Campus Universitário de Santiago, Aveiro, Portugal.
Tiago PedrosaCESAM & Laboratory of Biotechnology and Cytomics, Department of Biology, University of Aveiro, Campus Universitário de Santiago, Aveiro, Portugal.
Pedro PintoCESAM & Laboratory of Biotechnology and Cytomics, Department of Biology, University of Aveiro, Campus Universitário de Santiago, Aveiro, Portugal.
Catarina RemédiosCESAM & Laboratory of Biotechnology and Cytomics, Department of Biology, University of Aveiro, Campus Universitário de Santiago, Aveiro, Portugal.
Helena OliveiraCESAM & Laboratory of Biotechnology and Cytomics, Department of Biology, University of Aveiro, Campus Universitário de Santiago, Aveiro, Portugal.
Francisco PimentelLenitudes, Lisboa, Portugal; Faculty of Health Sciences, University Fernando Pessoa, R. Carlos da Maia 296, Porto, Portugal; Center for Health Studies & Research, University of Coimbra, Avenida Dias da Silva, Coimbra, Portugal; Faculdade de Ciências da Saúde - Universidade da Beira Interior, Avenida Infante D. Henrique, Covilhã, Portugal.
Luís AlmeidaLuzitin SA, R. Bayer 16, Coimbra, Portugal; Blueclinical Phase I, R. Sarmento de Beires 153, Porto, Portugal.
Conceição SantosCESAM & Laboratory of Biotechnology and Cytomics, Department of Biology, University of Aveiro, Campus Universitário de Santiago, Aveiro, Portugal.
University of Aveiro · PTLuzitin (Portugal) · PTUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sulforaphane (SFN) is a naturally-occurring isothiocyanate best known for its role as an indirect antioxidant. Notwithstanding, in different cancer cell lines, SFN may promote the accumulation of reactive oxygen species (ROS) and cause cell death e.g. by apoptosis. Osteosarcoma often becomes chemoresistant, and new molecular targets to prevent drug resistance are needed. Here, we aimed to determine the effect of SFN on ROS levels and to identify key biomarkers leading to ROS unbalance and apoptosis in the p53-null MG-63 osteosarcoma cell line. MG-63 cells were exposed to SFN for up to 48 h. At 10 μM concentration or higher, SFN decreased cell viability, increased the%early apoptotic cells and increased caspase 3 activity. At these higher doses, SFN increased ROS levels, which correlated with apoptotic endpoints and cell viability decline. In exposed cells, gene expression analysis revealed only partial induction of phase-2 detoxification genes. More importantly, SFN inhibited ROS-scavenging enzymes and impaired glutathione recycling, as evidenced by inhibition of glutathione reductase (GR) activity and combined inhibition of glutathione peroxidase (GPx) gene expression and enzyme activity. In conclusion, SFN induced oxidative stress and apoptosis via a p53-independent mechanism. GPx expression and activity were found associated with ROS accumulation in MG-63 cells and are potential biomarkers for the efficacy of ROS-inducing agents e.g. as co-adjuvant drugs in osteosarcoma.

Indexed as

AntioxidantsApoptosisBiomarkers, TumorCell Line, TumorCell SurvivalEnzyme InhibitorsGlutathioneHumansIntracellular SpaceIsothiocyanatesOsteosarcomaOxidative StressSulfoxidesTime FactorsAntioxidantsBiomarkers, TumorEnzyme InhibitorsGlutathioneIsothiocyanatessulforaphaneSulfoxides

Identifiers

PMID24667842
PMCPMC3965485
OpenAlexW2095200952

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.