Evidence map›Paper›PMID 29430283›Full record

ReviewOxidative medicine and cellular longevity2017

Possible Mechanisms of Mercury Toxicity and Cancer Promotion: Involvement of Gap Junction Intercellular Communications and Inflammatory Cytokines.

Roberto Zefferino, Claudia Piccoli, Nunzia Ricciardi, Rosella Scrima, Nazzareno Capitanio

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 3 pooled it
2.5field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 3 syntheses or guidelines pooled it, 76 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Roberto ZefferinoDepartment of Medical and Surgical Sciences, University of Foggia, Via L. Pinto 1, 71122 Foggia, Italy.ORCID 0000-0001-9398-7139
Claudia PiccoliDepartment of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto 1, 71122 Foggia, Italy.
Nunzia RicciardiDepartment of Medical and Surgical Sciences, University of Foggia, Via L. Pinto 1, 71122 Foggia, Italy.
Rosella ScrimaDepartment of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto 1, 71122 Foggia, Italy.
Nazzareno CapitanioDepartment of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto 1, 71122 Foggia, Italy.
University of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A number of observations indicate that heavy metals are able to alter cellular metabolic pathways through induction of a prooxidative state. Nevertheless, the outcome of heavy metal-mediated effects in the development of human diseases is debated and needs further insights. Cancer is a well-established DNA mutation-linked disease; however, epigenetic events are perhaps more important and harmful than genetic alterations. Unfortunately, we do not have reliable screening methods to assess/validate the epigenetic (promoter) effects of a physical or a chemical agent. We propose a mechanism of action whereby mercury acts as a possible promoter carcinogen. In the present contribution, we resume our previous studies on mercury tested at concentrations comparable with its occurrence as environmental pollutant. It is shown that Hg(II) elicits a prooxidative state in keratinocytes linked to inhibition of gap junction-mediated intercellular communication and proinflammatory cytokine production. These combined effects may on one hand isolate cells from tissue-specific homeostasis promoting their proliferation and on the other hand tamper the immune system defense/surveillance checkmating the whole organism. Since Hg(II) is not a mutagenic/genotoxic compound directly affecting gene expression, in a broader sense, mercury might be an example of an epigenetic tumor promoter or, further expanding this concept, a "metagenetic" effector.

Indexed as

Cell CommunicationCytokinesGap JunctionsHumansMercuryNeoplasmsCytokinesMercury

Identifiers

PMID29430283
PMCPMC5752980
OpenAlexW2781026892

What OpenQuestion holds

Textmetadata
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.