Document Detail


Mercury modulates interplay between IL-1beta, TNF-alpha, and gap junctional intercellular communication in keratinocytes: mitigation by lycopene.
MedLine Citation:
PMID:  19404869     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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, TNFalpha and IL-1beta 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 TNFalpha and IL-1beta 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-1beta and TNFalpha that had been significantly reduced within--keratinocytes that had been pre-treated for 24 hr with 10 nM HgCl(2). 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.
Authors:
Roberto Zefferino; Antonella Leone; Simona Piccaluga; Raffaele Cincione; Luigi Ambrosi
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of immunotoxicology     Volume:  5     ISSN:  1547-6901     ISO Abbreviation:  J Immunotoxicol     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2009-04-30     Completed Date:  2009-06-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101201960     Medline TA:  J Immunotoxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  353-60     Citation Subset:  IM    
Affiliation:
Department of Medical and Occupational Sciences, University of Foggia, Italy. r.zefferino@unifg.it
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MeSH Terms
Descriptor/Qualifier:
Anticarcinogenic Agents / pharmacology
Carotenoids / pharmacology*
Cell Communication / drug effects*
Cells, Cultured
Gap Junctions / drug effects*,  metabolism
Humans
Interleukin-1beta / metabolism*
Keratinocytes / drug effects*,  metabolism
Lipopolysaccharides / pharmacology
Lycopersicon esculentum / chemistry
Mercuric Chloride / pharmacology
Mercury / pharmacology*
Plant Extracts / pharmacology
Tumor Necrosis Factor-alpha / metabolism*
Chemical
Reg. No./Substance:
0/Anticarcinogenic Agents; 0/Interleukin-1beta; 0/Lipopolysaccharides; 0/Plant Extracts; 0/Tumor Necrosis Factor-alpha; 0/oleoresins; 36-88-4/Carotenoids; 502-65-8/lycopene; 7439-97-6/Mercury; 7487-94-7/Mercuric Chloride

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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