Characterization of programmed cell death induced by oxidative stress in selenium - deficient hepatocellular carcinoma cells

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buir.advisorÖztürk, Mehmet
dc.contributor.authorİnce, Gülayşe
dc.date.accessioned2016-01-08T20:16:44Z
dc.date.available2016-01-08T20:16:44Z
dc.date.issued1999
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.descriptionAnkara : Department of Molecular Biology and Genetics and Institute of Engineering and Science, Bilkent Univ., 1999.en_US
dc.descriptionThesis (Master's) -- Bilkent University, 1999.en_US
dc.descriptionIncludes bibliographical references leaves 64-72en_US
dc.description.abstractSelenium (Se) plays an important role in eliminating the reactive oxygen species generated during oxidative stress. Se-containing selenocysteine is an essential amino acid required for the synthesis of many selenoproteins, such as glutathione peroxidase. Se-dependent glutathione peroxidase is the major en2yme that metabolizes organic and hydrogen peroxides in the cell. It appears that Se manifests its antioxidant effect through the selenoproteins. Se deficiency causes a wide range of pathological conditions. Keshan disease, characterized by cardiomyocyte and liver cell death, defined as "necrosis", was found to be associated with Se deficiency. Se deficiency is also observed in liver cirrhosis, alcoholic liver disease, HIV positive and AIDS patients, thyroid hormone abnormalities, etc. Moreover, epidemiological studies show that Se deficiency increases the risk of many cancer types, including hepatocellular carcinoma (HCC). The molecular mechanisms of the pathologies associated with Se deficiency are mostly unknown. In this study, the in vitro responses of human hepatocellular carcinoma cells, to Se deficiency have been examined. Apoptotic changes (nuclear condensation, positive annexin V staining, genomic DNA breaks) are detected in Huh7, HepG2, and Mahlavu cells under Se-deficient culture conditions. Hydrogen peroxide addition into the culture medium aggravates apoptosis. Such changes are prevented by the supplementation of Se. The Se-dependent glutathione peroxidase enzyme is shown to be reduced in cells grown under Se-deficient conditions, explaining the build up of intracellular oxidative stress. It is proposed that the cell death observed in many pathologies associated with Se deficiency, is the result of the programmed cell death, triggered by an increase in intracellular oxidative stress, as opposed to necrotic cell death. Hep3B, Hep3B-TR, Hep40, PLC/PRF/5 and BC1/R14 cell lines have not displayed cell death when grown in Se-deficient conditions and were resistant to hydrogen peroxide, as well. The presence of such cell lines and the differential sensitivities manifested by HepG2, Huh7 and Mahlavu suggest a complete or partial gained resistance for apoptosis, which may contribute to the onset or progression of HCC, consistent with the increased risk of HCC in Se deficiency.en_US
dc.description.degreeM.S.en_US
dc.description.statementofresponsibilityİnce, Gülayşeen_US
dc.format.extent72 leaves, illustrationsen_US
dc.identifier.urihttp://hdl.handle.net/11693/18156
dc.language.isoEnglishen_US
dc.publisherBilkent Universityen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectSeleniumen_US
dc.subjectGlutathione peroxidaseen_US
dc.subjectHydrogen Peroxideen_US
dc.subjectOxidative Stressen_US
dc.subjectApoptosisen_US
dc.subjectHepatocellular Carcinomaen_US
dc.subject.lccQV138.S5 I53 1999en_US
dc.subject.lcshSelenium--Physiological effect.en_US
dc.subject.lcshSelenium--Health aspects.en_US
dc.titleCharacterization of programmed cell death induced by oxidative stress in selenium - deficient hepatocellular carcinoma cellsen_US
dc.typeThesisen_US

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Dept. of Molecular Biology and Genetics - Master's degree