{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/86646"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/86646","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"The Mechanism of Oxygen and Nitric Oxide Toxicity in Escherichia Coli","abstract":"The presence of nitric oxide (NO) greatly accelerates the rate at which hydrogen peroxide (H2O2) kills E. coli. The goal of this study was to determine the mechanism of this synergism. The filamentation of the dead cells, and their protection by cell-permeable iron chelators, indicated that NO/H2O2 killed cells by damaging their DNA through the Fenton reaction. NO also blocked respiration, an event which previous studies have shown can stimulate oxidative DNA damage. The resultant accumulation of NADH accelerates the reduction of free flavins by flavin reductase, and these reduced flavins drive Fenton chemistry by tranferring electrons to free iron. The possibility that H2O2 and NO synergize when macrophages attack captive bacteria is discussed.","abstract_html":"The presence of nitric oxide (NO) greatly accelerates the rate at which hydrogen peroxide (H2O2) kills E. coli. The goal of this study was to determine the mechanism of this synergism. The filamentation of the dead cells, and their protection by cell-permeable iron chelators, indicated that NO/H2O2 killed cells by damaging their DNA through the Fenton reaction. NO also blocked respiration, an event which previous studies have shown can stimulate oxidative DNA damage. The resultant accumulation of NADH accelerates the reduction of free flavins by flavin reductase, and these reduced flavins drive Fenton chemistry by tranferring electrons to free iron. The possibility that H2O2 and NO synergize when macrophages attack captive bacteria is discussed.","abstract_has_math":false,"creators":["Woodmansee, Anh Nguyen"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Microbiology","degree_department":null,"school":null,"contributors":["Imlay, James A."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-28T15:17:09Z","date_published":"2015-09-28T15:17:09Z","updated_at":"2026-07-22T22:26:27Z","subjects":["Biology, Microbiology"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3070482"],"render_values":[{"text":"(MiAaPQ)AAI3070482","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/86646","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Imlay, James A."]},{"key":"dc:creator","label":"Author","values":["Woodmansee, Anh Nguyen"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-28T15:17:09Z","10000-01-01","2002"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Microbiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Microbiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/86646","(MiAaPQ)AAI3070482"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The presence of nitric oxide (NO) greatly accelerates the rate at which hydrogen peroxide (H2O2) kills E. coli. The goal of this study was to determine the mechanism of this synergism. The filamentation of the dead cells, and their protection by cell-permeable iron chelators, indicated that NO/H2O2 killed cells by damaging their DNA through the Fenton reaction. NO also blocked respiration, an event which previous studies have shown can stimulate oxidative DNA damage. The resultant accumulation of NADH accelerates the reduction of free flavins by flavin reductase, and these reduced flavins drive Fenton chemistry by tranferring electrons to free iron. The possibility that H2O2 and NO synergize when macrophages attack captive bacteria is discussed.","Made available in DSpace on 2015-09-28T15:17:09Z (GMT). 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The goal of this study was to determine the mechanism of this synergism. The filamentation of the dead cells, and their protection by cell-permeable iron chelators, indicated that NO/H2O2 killed cells by damaging their DNA through the Fenton reaction. NO also blocked respiration, an event which previous studies have shown can stimulate oxidative DNA damage. The resultant accumulation of NADH accelerates the reduction of free flavins by flavin reductase, and these reduced flavins drive Fenton chemistry by tranferring electrons to free iron. The possibility that H2O2 and NO synergize when macrophages attack captive bacteria is discussed.","Made available in DSpace on 2015-09-28T15:17:09Z (GMT). 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