Evidence map›Paper›PMID 21994240›Full record

ArticleInternational journal of toxicology2011

Novel lipid-soluble thiol-redox antioxidant and heavy metal chelator, N,N'-bis(2-mercaptoethyl)isophthalamide (NBMI) and phospholipase D-specific inhibitor, 5-fluoro-2-indolyl des-chlorohalopemide (FIPI) attenuate mercury-induced lipid signaling leading to protection against cytotoxicity in aortic endothelial cells.

Jordan D Secor, Sainath R Kotha, Travis O Gurney, Rishi B Patel, Nicholas R Kefauver, Niladri Gupta, Andrew J Morris, Boyd E Haley, Narasimham L Parinandi

Open access · greenAbstract read
In one paragraph

Article in International journal of toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Trial
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  10. Thimerosal exposure and the role of sulfation chemistry and thiol availability in autism.International journal of environmental research and public health · 2013
    Review
  11. Article
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.

Jordan D SecorLipid Signaling, Lipidomics, and Vasculotoxicity Laboratory, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Dorothy M. Davis Heartand Lung Research Institute and Division of Pharmacology, Colleges of Medicineand Pharmacy, The Ohio State University, Columbus, OH, USA.
Sainath R Kotha
Travis O Gurney
Rishi B Patel
Nicholas R Kefauver
Niladri Gupta
Andrew J Morris
Boyd E Haley
Narasimham L Parinandi
American Association of Colleges of Pharmacy · USThe Ohio State University · USUniversity of Kentucky · US

Funding

Intermittent hypoxia, adiponectin, and insulin resistance in cardiovascular riskR01HL093463 · NHLBI · OHIO STATE UNIVERSITY · PI MAGALANG, ULYSSES J, PARINANDI, NARASIMHAM LAXMI · 2010 to 2013
$1.5M
NHLBI NIH HHS HL093463NHLBI NIH HHS R01 HL093463
6 · The paper itself

Abstract

Here, we investigated thiol-redox-mediated phospholipase D (PLD) signaling as a mechanism of mercury cytotoxicity in mouse aortic endothelial cell (MAEC) in vitro model utilizing the novel lipid-soluble thiol-redox antioxidant and heavy metal chelator, N,N'-bis(2-mercaptoethyl)isophthalamide (NBMI) and the novel PLD-specific inhibitor, 5-fluoro-2-indolyl des-chlorohalopemide (FIPI). Our results demonstrated (i) mercury in the form of mercury(II) chloride, methylmercury, and thimerosal induced PLD activation in a dose- and time-dependent manner; (ii) NBMI and FIPI completely attenuated mercury- and oxidant-induced PLD activation; (iii) mercury induced upstream phosphorylation of extracellular-regulated kinase 1/2 (ERK1/2) leading to downstream threonine phosphorylation of PLD(1) which was attenuated by NBMI; (iv) mercury caused loss of intracellular glutathione which was restored by NBMI; and (v) NBMI and FIPI attenuated mercury- and oxidant-induced cytotoxicity in MAECs. For the first time, this study demonstrated that redox-dependent and PLD-mediated bioactive lipid signaling was involved in mercury-induced vascular EC cytotoxicity which was protected by NBMI and FIPI.

Indexed as

AnimalsAntioxidantsAortaCells, CulturedCell SurvivalChelating AgentsDomperidoneEndothelial CellsEnvironmental PollutantsEnzyme InhibitorsIndolesLipid MetabolismL-Lactate DehydrogenaseMercuryMiceOxidation-Reduction5-fluoro-2-indolyldeschlorohalopemideAntioxidantsChelating AgentsDomperidoneEnvironmental PollutantsEnzyme InhibitorsIndolesL-Lactate DehydrogenaseMercuryPhospholipase DPhthalic AcidsSulfhydryl Compounds

Identifiers

PMID21994240
PMCPMC3503146
OpenAlexW2045995572

What OpenQuestion holds

Textmetadata
LicenceTDM
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.