Evidence map›Paper›PMID 29376053›Full record

ArticleFrontiers in medicine2017

Metabolic Linkage and Correlations to Storage Capacity in Erythrocytes from Glucose 6-Phosphate Dehydrogenase-Deficient Donors.

Julie A Reisz, Vassilis L Tzounakas, Travis Nemkov, Artemis I Voulgaridou, Issidora S Papassideri, Anastasios G Kriebardis, Angelo D'Alessandro, Marianna H Antonelou

Open access · goldAbstract read
In one paragraph

Article in Frontiers in medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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  19. Sex-related aspects of the red blood cell storage lesion.Blood transfusion = Trasfusione del sangue · 2021
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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

8 authors at 3 institutions in 2 countries.

Julie A ReiszDepartment of Biochemistry and Molecular Genetics, School of Medicine, University of Colorado, Aurora, CO, United States.
Vassilis L TzounakasDepartment of Biology, School of Science, National and Kapodistrian University of Athens, Athens, Greece.
Travis NemkovDepartment of Biochemistry and Molecular Genetics, School of Medicine, University of Colorado, Aurora, CO, United States.
Artemis I Voulgaridou"Apostle Paul" Educational Institution, Thessaloniki, Greece.
Issidora S PapassideriDepartment of Biology, School of Science, National and Kapodistrian University of Athens, Athens, Greece.
Anastasios G KriebardisDepartment of Medical Laboratories, Faculty of Health and Caring Professions, Technological and Educational Institute of Athens, Athens, Greece.
Angelo D'AlessandroDepartment of Biochemistry and Molecular Genetics, School of Medicine, University of Colorado, Aurora, CO, United States.
Marianna H AntonelouDepartment of Biology, School of Science, National and Kapodistrian University of Athens, Athens, Greece.
National and Kapodistrian University of Athens · GRUniversity of Colorado Anschutz Medical Campus · USTechnological Educational Institute of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIn glucose 6-phosphate dehydrogenase (G6PD) deficiency, decreased NADPH regeneration in the pentose phosphate pathway and subnormal levels of reduced glutathione result in insufficient antioxidant defense, increased susceptibility of red blood cells (RBCs) to oxidative stress, and acute hemolysis following exposure to pro-oxidant drugs and infections. Despite the fact that redox disequilibrium is a prominent feature of RBC storage lesion, it has been reported that the G6PD-deficient RBCs store well, at least in respect to energy metabolism, but their overall metabolic phenotypes and molecular linkages to the storability profile are scarcely investigated.

methodsWe performed UHPLC-MS metabolomics analyses of weekly sampled RBC concentrates from G6PD sufficient and deficient donors, stored in citrate phosphate dextrose/saline adenine glucose mannitol from day 0 to storage day 42, followed by statistical and bioinformatics integration of the data.

resultsOther than previously reported alterations in glycolysis, metabolomics analyses revealed bioactive lipids, free fatty acids, bile acids, amino acids, and purines as top variables discriminating RBC concentrates for G6PD-deficient donors. Two-way ANOVA showed significant changes in the storage-dependent variation in fumarate, one-carbon, and sulfur metabolism, glutathione homeostasis, and antioxidant defense (including urate) components in G6PD-deficient vs. sufficient donors. The levels of free fatty acids and their oxidized derivatives, as well as those of membrane-associated plasticizers were significantly lower in G6PD-deficient units in comparison to controls. By using the strongest correlations between

conclusionThe metabolic phenotypes of G6PD-deficient donors recapitulate the basic storage lesion profile that leads to loss of metabolic linkage and rewiring. Donor-related issues affect the storability of RBCs even in the narrow context of this donor subgroup in a way likely relevant to transfusion medicine.

Indexed as

donor variationglucose 6-phosphate dehydrogenase deficiencyinteractomemass spectrometrymetabolomicsred blood cell storage lesiontransfusion medicine

Identifiers

PMID29376053
PMCPMC5768619
OpenAlexW2783257071

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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.