Evidence map›Paper›PMID 19549508›Full record

ArticleBiochemical pharmacology2009

PCB-induced endothelial cell dysfunction: role of poly(ADP-ribose) polymerase.

Simon G Helyar, Bella Patel, Kevin Headington, Mary El Assal, Prabal K Chatterjee, Pal Pacher, Jon G Mabley

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Key Characteristics of Cardiovascular Toxicants.Environmental health perspectives · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Exercise protects against PCB-induced inflammation and associated cardiovascular risk factors.Environmental science and pollution research international · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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

7 authors at 3 institutions in 2 countries.

Simon G HelyarBrighton and Sussex Medical School, Falmer, Brighton BN1 9PH, UK.
Bella Patel
Kevin Headington
Mary El Assal
Prabal K Chatterjee
Pal Pacher
Jon G Mabley
University of Brighton · GBBrighton and Sussex Medical School · GBNational Institute on Alcohol Abuse and Alcoholism · US

Funding

Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZ01AA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2006 to 2008
$1.3M
Intramural NIH HHS Z01 AA000375Intramural NIH HHS Z99 AA999999
6 · The paper itself

Abstract

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants implicated in the development of pro-inflammatory events critical in the pathology of atherosclerosis and cardiovascular disease. PCB exposure of endothelial cells results in increased cellular oxidative stress, activation of stress and inflammatory pathways leading to increased expression of cytokines and adhesion molecules and ultimately cell death, all of which can lead to development of atherosclerosis. To date no studies have been performed to examine the direct effects of PCB exposure on the vasculature relaxant response which if impaired may predispose individuals to hypertension, an additional risk factor for atherosclerosis. Overactivation of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP) following oxidative/nitrosative stress in endothelial cells and subsequent depletion of NADPH has been identified as a central mediator of cellular dysfunction. The aim therefore was to investigate whether 2,2',4,6,6'-pentachlorobiphenyl (PCB 104) directly causes endothelial cell dysfunction via increased oxidative stress and subsequent overactivation of PARP. Exposure of ex vivo rat aortic rings to PCB 104 impaired the acetylcholine-mediated relaxant response, an effect that was dependent on both concentration and exposure time. In vitro exposure of mouse endothelial cells to PCB 104 resulted in increased cellular oxidative stress through activation of the cytochrome p450 enzyme CYP1A1 with subsequent overactivation of PARP and NADPH depletion. Pharmacological inhibition of CYP1A1 or PARP protected against the PCB 104-mediated endothelial cell dysfunction. In conclusion, the environmental contaminants, PCBs, can activate PARP directly impairing endothelial cell function that may predispose exposed individuals to development of hypertension and cardiovascular disease.

Indexed as

AcetylcholineAnimalsAorta, ThoracicCells, CulturedCell SurvivalCytochrome P-450 CYP1A1Dose-Response Relationship, DrugEndothelial CellsEndothelium, VascularEnvironmental PollutantsIndicators and ReagentsMaleMiceMolecular StructureMuscle, Smooth, VascularNADP2,2',4,6,6'-pentachlorobiphenylAcetylcholineCytochrome P-450 CYP1A1Environmental PollutantsIndicators and ReagentsNADPNitric OxideNitroblue TetrazoliumOxidantsPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesPolychlorinated Biphenyls

Identifiers

PMID19549508
PMCPMC2756480
OpenAlexW1969253172

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.