http://www.cnr.it/ontology/cnr/individuo/prodotto/ID179398

Mercury modulates interplay between IL-1a, TNF-b, and gap junctional intercellular communication in keratinocytes: mitigation by lycopene (Articolo in rivista)

Type

Articolo in rivista (Classe)
Prodotto della ricerca (Classe)

Label

Mercury modulates interplay between IL-1a, TNF-b, and gap junctional intercellular communication in keratinocytes: mitigation by lycopene (Articolo in rivista) (literal)

Anno

2008-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1080/15476910802482854 (literal)

Alternative label

Zefferino R; Leone A; Piccaluga S; Cincione R; Ambrosi L; (2008)
Mercury modulates interplay between IL-1a, TNF-b, and gap junctional intercellular communication in keratinocytes: mitigation by lycopene
in Journal of immunotoxicology (Print); Taylor & Francis Inc., Philadelphia (Stati Uniti d'America)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Zefferino R; Leone A; Piccaluga S; Cincione R; Ambrosi L; (literal)

Pagina inizio

353 (literal)

Pagina fine

360 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url

http://informahealthcare.com/doi/abs/10.1080/15476910802482854 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

5 (literal)

Rivista

Journal of immunotoxicology (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

8 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

4 (literal)

Note

Google Scholar (literal)
Scopus (literal)
PubMe (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

Department of Medical and Occupational Sciences, University of Foggia, Italy CNR, Italian National Research Council-ISPA-LECCE, Italy Department of Biomedical Sciences, University of Foggia, Italy S. Maugeri Foundation, Cassano Delle Murge (BA), Italy (literal)

Titolo

Mercury modulates interplay between IL-1a, TNF-b, and gap junctional intercellular communication in keratinocytes: mitigation by lycopene (literal)

Abstract

Gap junctional intercellular communication (GJIC) is used to control cell proliferation. It is not surprising then that a lack of GJIC (i.e., during loss of contact inhibition among adjacent cells) is associated with cancer promotion/progression. There also seems to be a link between ineffective GJIC and increases in inflammatory events. Interestingly, many cytokines released during an inflammatory response also have critical roles in cancer cell survival. Specifically, TNF? and IL-1? are important for initiating/augmenting CD8+- and NK-cell mediated killing; however, in what appears counterintuitive, each--at times--can act to protect cancer cells against apoptosis, a major mechanism for cell killing from within. It is thus plausible to assume that certain toxicants might act as cancer promoters in manners distinct from/augmentive of direct effects on DNA, i.e., by concurrently altering GJIC and cytokine formation in host or microenvironment of a cancer cell. Our research has evaluated effects of many toxicants upon keratinocytes; in particular, we have examined effects of mercury on GJIC and on TNF? and IL-1? levels in (and secretion by) these cells. In the studies here, a tomato preparation (i.e., an oleoresin) bearing the antioxidant carotenoid lycopene was examined for its effects on GJIC and cytokine formation by keratinocytes in general, and its potential ability to mitigate/ reverse the toxic effects of mercury in the cells in particular. It was shown that a 4-hr treatment with the oleoresin (containing 56, 6 nM lycopene) re-established GJIC among--and increased the formation of IL-1? and TNF? that had been significantly reduced within--keratinocytes that had been pre-treated for 24 hr with 10 nM HgCl2. These results show that effects of mercury likely depend on some level of oxidative stress and that its potential effects on keratinocyte GJIC and cytokine concentrations could, in an exposed host, be mitigated/reversed by increased dietary intake of carotenoids like lycopene. (literal)

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