Linked Life Data

15453640

Source:http://linkedlifedata.com/resource/pubmed/id/15453640

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SubjectPredicateObjectContext
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pubmed-article:15453640pubmed:dateCreated2004-9-29lld:pubmed
pubmed-article:15453640pubmed:abstractTextExpression of multiple drug resistant (MDR) phenotype and over-expression of P-glycoprotein (P-gp) in the human hepatocellular carcinoma (HCC) cell clone P1(0.5), derived from the PLC/PRF/5 cell line (P5), are associated with strong resistance to oxidative stress and a significant (p < 0.01) increase in intracellular vitamin E content as compared with the parental cell line. This study evaluates the role of vitamin E in conferring resistance to drugs and oxidative stress in P1(0.5) cells. Parental drug-sensitive cells, P5, were incubated in alpha-tocopherol succinate (alpha-TS, 5 microM for 24 h) enriched medium to increase intracellular vitamin E content to levels comparable to those observed in P1(0.5) cells at basal conditions. Susceptibility to lipid peroxidation and oxidative DNA damage were assessed by measuring the concentration of thiobarbituric-reactive substances (TBARS) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) at basal and after experimental conditions. Cell capacity to form colonies and resistance to doxorubicin were also studied. P5 cells, treated with alpha-TS, became resistant to ADP-Fe3+ and to ionizing radiation-induced lipid peroxidation as P1(0.5) cells. Exposure to ADP-Fe3+ or ionizing radiation increased TBARS and the 8-OHdG content in the P5 cells, while vitamin E enrichment abolished these effects. Irradiation doses at 5 cGy increased TBARS and 8-OHdG. They also inhibited cell capacity to form colonies in the untreated P5 cells. Incubation with alpha-TS fully reverted this effect and significantly (p < 0.01) reduced the inhibitory effect of cell proliferation induced by irradiation doses at >500 cGy. Resistance to doxorubicin was not affected by alpha-TS. These observations demonstrate the role of vitamin E in conferring protection from lipid peroxidation, ionizing radiation and oxidative DNA damage on the human HCC cell line. They also rule out any role of P-gp over-expression as being responsible for these observations in cells with MDR phenotype expression.lld:pubmed
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pubmed-article:15453640pubmed:authorpubmed-author:FantappièOrne...lld:pubmed
pubmed-article:15453640pubmed:authorpubmed-author:SolazzoMichel...lld:pubmed
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pubmed-article:15453640pubmed:volume38lld:pubmed
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pubmed-article:15453640pubmed:pagination751-9lld:pubmed
pubmed-article:15453640pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:15453640pubmed:year2004lld:pubmed
pubmed-article:15453640pubmed:articleTitleVitamin E protects DNA from oxidative damage in human hepatocellular carcinoma cell lines.lld:pubmed
pubmed-article:15453640pubmed:affiliationDepartment of Internal Medicine, U.A. Oncologia, Azienda Ospedaliero-Universitaria Careggi, Viale G.B. Morgagni 85, I-50134 Florence, Italy.lld:pubmed
pubmed-article:15453640pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15453640pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed