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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 7028583, 6 pages
https://doi.org/10.1155/2017/7028583
Review Article

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

1Department of Medical and Surgical Sciences, University of Foggia, Via L. Pinto 1, 71122 Foggia, Italy
2Department of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto 1, 71122 Foggia, Italy

Correspondence should be addressed to Roberto Zefferino; ti.gfinu@onireffez.otrebor

Received 28 July 2017; Accepted 29 November 2017; Published 21 December 2017

Academic Editor: Pan Chen

Copyright © 2017 Roberto Zefferino et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.