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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
1991-12-19
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pubmed:abstractText |
We have previously demonstrated that diverse carotenoids inhibit chemically induced neoplastic transformation in 10T1/2 cells. To address their mechanism of action, the effects of six diverse carotenoids, with or without provitamin A activity, on gap junctional communication and lipid peroxidation have been investigated. beta-Carotene, canthaxanthin, lutein, lycopene and alpha-carotene increased gap junctional intercellular communication in a dose-dependent manner in the above order of potency, whereas m-bixin was inactive at concentrations up to 10(-5) M. alpha-Tocopherol, a potent chain-breaking antioxidant, caused a marginal enhancement of junctional communication. The enhancement of junctional communication by diverse carotenoids showed a strong statistical correlation with their previously determined ability to inhibit methylcholanthrene-induced neoplastic transformation (r = -0.75). All carotenoids tested inhibited lipid peroxidation, but with differing potencies. alpha-Tocopherol was the most active inhibitor followed by m-bixin. The capacity of carotenoids or alpha-tocopherol to inhibit lipid peroxidation was neither consistent with their ability to inhibit neoplastic transformation (r = 0.30) nor to increase junctional communication (r = 0.12). Since junctional communication appears to play an important role in cell growth control and carcinogenesis, we propose that in this system carotenoid-enhanced intercellular communication provides a mechanistic basis for the cancer chemopreventive action of carotenoids. These data also imply that carotenoids function in a manner analogous to retinoids in the 10T1/2 assay system. Interestingly this activity appears independent of their provitamin A status.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Canthaxanthin,
http://linkedlifedata.com/resource/pubmed/chemical/Carotenoids,
http://linkedlifedata.com/resource/pubmed/chemical/Lutein,
http://linkedlifedata.com/resource/pubmed/chemical/Vitamin E,
http://linkedlifedata.com/resource/pubmed/chemical/alpha-carotene,
http://linkedlifedata.com/resource/pubmed/chemical/beta Carotene,
http://linkedlifedata.com/resource/pubmed/chemical/bixin,
http://linkedlifedata.com/resource/pubmed/chemical/lycopene
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0143-3334
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2109-14
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1934296-Animals,
pubmed-meshheading:1934296-Canthaxanthin,
pubmed-meshheading:1934296-Carotenoids,
pubmed-meshheading:1934296-Cell Communication,
pubmed-meshheading:1934296-Cell Transformation, Neoplastic,
pubmed-meshheading:1934296-Lipid Peroxidation,
pubmed-meshheading:1934296-Lutein,
pubmed-meshheading:1934296-Mice,
pubmed-meshheading:1934296-Vitamin E,
pubmed-meshheading:1934296-beta Carotene
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pubmed:year |
1991
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pubmed:articleTitle |
Carotenoids enhance gap junctional communication and inhibit lipid peroxidation in C3H/10T1/2 cells: relationship to their cancer chemopreventive action.
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pubmed:affiliation |
Cancer Research Center of Hawaii, University of Hawaii, Honolulu 96813.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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