Evidence map›Paper›PMID 24891512›Full record

ArticleThe Journal of biological chemistry2014

Nitrosothiol formation and protection against Fenton chemistry by nitric oxide-induced dinitrosyliron complex formation from anoxia-initiated cellular chelatable iron increase.

Qian Li, Chuanyu Li, Harry K Mahtani, Jian Du, Aashka R Patel, Jack R Lancaster

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Insights on the endogenous labile iron pool binding properties.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
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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.

Qian LiFrom the Department of Anesthesiology and Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, qianli@uab.edu.
Chuanyu LiFrom the Department of Anesthesiology and Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294.
Harry K MahtaniFrom the Department of Anesthesiology and Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294.
Jian Duthe Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Anhui Medical University, Hefei 230032, China, and.
Aashka R PatelVestavia Hills High School, Vestavia Hills, Alabama 35216.
Jack R LancasterFrom the Department of Anesthesiology and Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294.

Funding

Biological Chemistry of Reactive Nitrogen Species Signaling in Cancer EtiologyR01CA131653 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LANCASTER, JACK R · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA-131653NCI NIH HHS R01 CA131653
6 · The paper itself

Abstract

Dinitrosyliron complexes (DNIC) have been found in a variety of pathological settings associated with (•)NO. However, the iron source of cellular DNIC is unknown. Previous studies on this question using prolonged (•)NO exposure could be misleading due to the movement of intracellular iron among different sources. We here report that brief (•)NO exposure results in only barely detectable DNIC, but levels increase dramatically after 1-2 h of anoxia. This increase is similar quantitatively and temporally with increases in the chelatable iron, and brief (•)NO treatment prevents detection of this anoxia-induced increased chelatable iron by deferoxamine. DNIC formation is so rapid that it is limited by the availability of (•)NO and chelatable iron. We utilize this ability to selectively manipulate cellular chelatable iron levels and provide evidence for two cellular functions of endogenous DNIC formation, protection against anoxia-induced reactive oxygen chemistry from the Fenton reaction and formation by transnitrosation of protein nitrosothiols (RSNO). The levels of RSNO under these high chelatable iron levels are comparable with DNIC levels and suggest that under these conditions, both DNIC and RSNO are the most abundant cellular adducts of (•)NO.

Indexed as

AnimalsCell HypoxiaCell LineDeferoxamineElectron Spin Resonance SpectroscopyHydrogen PeroxideIronIron Chelating AgentsMacrophagesMiceNitric OxideNitrogen OxidesReactive Oxygen SpeciesS-NitrosothiolsDeferoxaminedinitrosyl iron complexFenton's reagentHydrogen PeroxideIronIron Chelating AgentsNitric OxideNitrogen OxidesReactive Oxygen SpeciesS-NitrosothiolsChelatable IronDinitrosyliron ComplexesElectron Paramagnetic Resonance (EPR)Fenton ReactionHypoxiaIronNitric OxideNitrosothiolReactive Oxygen Species (ROS)Thiol

Identifiers

PMID24891512
PMCPMC4106312

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.