Evidence map›Paper›PMID 23874620›Full record

ArticlePloS one2013

Chronic cadmium treatment promotes oxidative stress and endothelial damage in isolated rat aorta.

Camila C P Almenara, Gilson B Broseghini-Filho, Marcus V A Vescovi, Jhuli K Angeli, Thaís de O Faria, Ivanita Stefanon, Dalton V Vassallo, Alessandra S Padilha

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
5.5field-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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.

  1. Pooled it
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  9. Metals, cardiovascular risk, and the interplay with oxidative stress: a mini-review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Review
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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 1 institution in 1 country.

Camila C P AlmenaraDepartment of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Espírito Santo, Brazil. camilaalmenaracp@gmail.com
Gilson B Broseghini-Filho
Marcus V A Vescovi
Jhuli K Angeli
Thaís de O Faria
Ivanita Stefanon
Dalton V Vassallo
Alessandra S Padilha
Universidade Federal do Espírito Santo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium is a highly toxic metal that is present in phosphate fertilizers, and the incidence of cadmium poisoning in the general population has increased, mainly due to cigarette smoking. Once absorbed, cadmium accumulates in the tissues, causing harmful effects including high blood pressure, endothelial damage and oxidative stress. Oxidative stress is known to efficiently produce oxidized low-density lipoprotein and consequently atherosclerosis, mainly in the aorta. However, the mechanisms through which endothelial damage is induced by cadmium have not been elucidated. Thus, the aim of this study was to investigate the effects of this metal in the isolated aorta and the possible role of oxidative stress. Rats received 100 mg.L(-1) cadmium chloride (CdCl2) in the drinking water or distilled water alone for four weeks. The pressor effect of cadmium was followed throughout the exposure period by tail plethysmography. At the end of the fourth week, the blood cadmium content was established, and the vascular reactivity of the isolated aorta to phenylephrine, acetylcholine and sodium nitroprusside was analyzed in the context of endothelium denudation and incubation with L-NAME, apocynin, losartan, enalapril, superoxide dismutase (SOD) or catalase. We observed an increased response to phenylephrine in cadmium-treated rats. This increase was abolished by catalase and SOD incubation. Apocynin treatment reduced the phenylephrine response in both treatment groups, but its effect was greater in cadmium-treated rats, and NOX2 expression was greater in the cadmium group. These results suggested that cadmium in blood concentrations similar to those found in occupationally exposed populations is able to stimulate NOX2 expression, contributing to oxidative stress and reducing NO bioavailability, despite enhanced eNOS expression. These findings suggest that cadmium exposure promotes endothelial damage that might contribute to inflammation, vascular injury and the development of atherosclerosis.

Indexed as

AcetophenonesAcetylcholineAnimalsAortaBlood PressureBody WeightCadmiumCatalaseDensitometryEnalaprilEndothelium, VascularIn Vitro TechniquesLosartanNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIINitroprussideAcetophenonesacetovanilloneAcetylcholineCadmiumCatalaseEnalaprilLosartanNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIINitroprussidePhenylephrineSuperoxide Dismutase

Identifiers

PMID23874620
PMCPMC3709967
OpenAlexW2037897244

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.