{"id":{"repo_id":"must-thes","oai_identifier":"oai:scholarsmine.mst.edu:doctoral_dissertations-2926"},"canonical_url":"https://search.dev.ndltd.org/etd/must-thes/oai:scholarsmine.mst.edu:doctoral_dissertations-2926","repository":{"repo_id":"must-thes","name":"Missouri University of Science and Technology","base_url":"https://scholarsmine.mst.edu/do/oai/"},"display":{"title":"Effects of combined exposure to ethanol and ionizing radiation on the antioxidant status of in vitro and in vivo models","abstract":"\"Ethanol and ionizing radiation exposure are independently known to cause tissue damage through various mechanisms. Non-enzymatic and enzymatic metabolism of ethanol, the latter via the cytochrome P₄₅₀2E1-dependent pathway, produces free radicals which deplete cellular glutathione (GSH). Ionizing radiation exposure has been shown to induce lipid peroxidation, DNA damage, protein oxidation, and GSH depletion, as well. It was postulated that initial exposure to ethanol, followed by ionizing radiation, would result in heightened oxidative stress. The in vitro model used in this investigation was HepG2 cells (human hepatocellular liver carcinoma cell line), while the in vivo model was Cd-1 mice\"--Abstract, page iii.","abstract_html":""Ethanol and ionizing radiation exposure are independently known to cause tissue damage through various mechanisms. Non-enzymatic and enzymatic metabolism of ethanol, the latter via the cytochrome P₄₅₀2E1-dependent pathway, produces free radicals which deplete cellular glutathione (GSH). Ionizing radiation exposure has been shown to induce lipid peroxidation, DNA damage, protein oxidation, and GSH depletion, as well. It was postulated that initial exposure to ethanol, followed by ionizing radiation, would result in heightened oxidative stress. The in vitro model used in this investigation was HepG2 cells (human hepatocellular liver carcinoma cell line), while the in vivo model was Cd-1 mice"--Abstract, page iii.","abstract_has_math":false,"creators":["Ogony, Joshua"],"institution":"University of Missouri--Rolla","degree_name":"Ph. D. in Chemistry","degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2016,"date_issued":"2016-02-10T08:00:00Z","date_published":"2016-02-10T08:00:00Z","updated_at":"2026-07-24T03:19:21Z","subjects":["Chemistry"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarsmine.mst.edu/doctoral_dissertations/1924","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Ogony, Joshua"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2016-02-10T08:00:00Z"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation - Open Access"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph. D. in Chemistry"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Missouri--Rolla"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Chemistry"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarsmine.mst.edu/doctoral_dissertations/1924"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["\"Ethanol and ionizing radiation exposure are independently known to cause tissue damage through various mechanisms. Non-enzymatic and enzymatic metabolism of ethanol, the latter via the cytochrome P₄₅₀2E1-dependent pathway, produces free radicals which deplete cellular glutathione (GSH). Ionizing radiation exposure has been shown to induce lipid peroxidation, DNA damage, protein oxidation, and GSH depletion, as well. It was postulated that initial exposure to ethanol, followed by ionizing radiation, would result in heightened oxidative stress. The in vitro model used in this investigation was HepG2 cells (human hepatocellular liver carcinoma cell line), while the in vivo model was Cd-1 mice\"--Abstract, page iii."]},{"key":"dc:title","label":"Title","values":["Effects of combined exposure to ethanol and ionizing radiation on the antioxidant status of in vitro and in vivo models"]}]}],"canonical_facts":{"dc:creator":["Ogony, Joshua"],"dc:date.available":["2016-02-10T08:00:00Z"],"dc:description.abstract":["\"Ethanol and ionizing radiation exposure are independently known to cause tissue damage through various mechanisms. Non-enzymatic and enzymatic metabolism of ethanol, the latter via the cytochrome P₄₅₀2E1-dependent pathway, produces free radicals which deplete cellular glutathione (GSH). Ionizing radiation exposure has been shown to induce lipid peroxidation, DNA damage, protein oxidation, and GSH depletion, as well. It was postulated that initial exposure to ethanol, followed by ionizing radiation, would result in heightened oxidative stress. The in vitro model used in this investigation was HepG2 cells (human hepatocellular liver carcinoma cell line), while the in vivo model was Cd-1 mice\"--Abstract, page iii."],"dc:identifier":["https://scholarsmine.mst.edu/doctoral_dissertations/1924"],"dc:subject":["Chemistry"],"dc:title":["Effects of combined exposure to ethanol and ionizing radiation on the antioxidant status of in vitro and in vivo models"],"dc:type":["Dissertation - Open Access"],"thesis:degree_name":["Ph. D. in Chemistry"],"thesis:institution_name":["University of Missouri--Rolla"]},"updated_at":"2026-07-24T03:19:21Z"}