Evidence map›Paper›PMID 27454767›Full record

ArticleRedox biology2016

Diabetes-induced oxidative stress in the vitreous humor.

Zsuzsanna Géhl, Edina Bakondi, Miklós D Resch, Csaba Hegedűs, Katalin Kovács, Petra Lakatos, Antal Szabó, Zoltán Nagy, László Virág

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  18. Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2019
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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.

Zsuzsanna GéhlDepartment of Ophthalmology, Semmelweis University, Budapest, Hungary.
Edina BakondiDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Miklós D ReschDepartment of Ophthalmology, Semmelweis University, Budapest, Hungary.
Csaba HegedűsDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Katalin KovácsDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary; MTA-DE Cell Biology and Signaling Research Group of the Hungarian Academy of Sciences, Debrecen, Hungary.
Petra LakatosDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Antal SzabóDepartment of Ophthalmology, Semmelweis University, Budapest, Hungary.
Zoltán NagyDepartment of Ophthalmology, Semmelweis University, Budapest, Hungary.
László VirágDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary; MTA-DE Cell Biology and Signaling Research Group of the Hungarian Academy of Sciences, Debrecen, Hungary. Electronic address: lvirag@med.unideb.hu.
Semmelweis University · HUUniversity of Debrecen · HUHungarian Academy of Sciences · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDiabetes is accompanied by fundamental rearrangements in redox homeostasis. Hyperglycemia triggers the production of reactive oxygen and nitrogen species which contributes to tissue damage in various target organs. Proliferative diabetic retinopathy (PDR) is a common manifestation of diabetic complications but information on the possible role of reactive intermediates in this condition with special regard to the involvement of the vitreous in PDR-associated redox alterations is scarce. The aim of the study was to determine key parameters of redox homeostasis [advanced glycation endproducts (AGE); protein carbonyl and glutathione (GSH)] content in the vitreous in PDR patients.

methodsThe study population involved 10 diabetic patients undergoing surgery for complications of proliferative diabetic retinopathy and 8 control (non-diabetic) patients who were undergoing surgery for epiretinal membranes. Vitreal fluids were assayed for the above biochemical parameters.

resultsWe found elevated levels of AGE in the vitreous of PDR patients (812.10 vs 491.69ng AGE/mg protein). Extent of protein carbonylation was also higher in the samples of diabetic patients (2.08 vs 0.67A/100μg protein). The GSH content also increased in the vitreous of PDR patients as compared to the control group (4.54 vs 2.35μmol/μg protein), respectively.

conclusionThe study demonstrates that diabetes-associated redox alterations also reach the vitreous with the most prominent changes being increased protein carbonylation and increased antioxidant levels.

Indexed as

Oxidative StressAdultAgedAged, 80 and overAntioxidantsDiabetic RetinopathyFemaleGlutathioneGlycation End Products, AdvancedHumansMaleMiddle AgedProtein CarbonylationVitreous BodyAntioxidantsGlutathioneGlycation End Products, AdvancedAdvanced glycation endproductsAntioxidantsDiabetesGlutathionProtein carbonylationProtein oxidationVitreous

Identifiers

PMID27454767
PMCPMC4961280
OpenAlexW2472238533

What OpenQuestion holds

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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.