Ozone is a major component of photochemical smog. High levels of this pollutant, sufficient to affect human health are found in many urban areas worldwide. Though limited studies in humans are supported by extensive findings from animal experiments, a difficulty in interpreting the results of these experiments has lead to an ambiguity on the biochemical mechanism of ozone toxicity. To elucidate the mechanism by which ozone causes cell damage and eventual cell death we conducted a comprehensive study using Escherichia coli K-12 as a model.
Studies on the comparative inactivation of bacteriophage lambda (λ), Escherichia coli, and Candida albicans showed that λ was significantly more sensitive to ozone, in buffered solutions. The quenching effect of antioxidants in body fluids decreased the inactivation rate of λ. Short interval exposure of E. coli K-12 transformed with pACYC184 plasmid DNA resulted in protein and nucleic acid leakage and production of thiobarbituric acid reactive substances, without affecting cell viability. The intracellular components, protein and plasmid DNA, remained intact. The enzymes malate dehydrogenase, lactate dehydrogenase and glutathione disulfide reductase were unaffected, while glyceraldehyde-3-phosphate dehydrogenase activity decreased significantly. Glutathione and total sulfhydryl compounds were also very sensitive to ozone oxidation. With longer duration of ozone exposure cell viability decreased with a more significant increase in lipid oxidation and protein and nucleic acid leakage. The total intracellular proteins and plasmid DNA showed progressive degradation corresponding to the decrease in cell viability.
Cell survival, induction of lipid oxidation and intracellular protein and DNA damage in two strains of E. coli K-12 (recA and wild type) were shown to be equally susceptible to ozone. Rec A protein levels decreased subsequent to ozone exposure indicating that this enzyme is not involved in the DNA repair process after ozone-induced damage. The membrane components are the primary targets of ozone damage with subsequent reactions involving the intracellular components, protein and DNA. The sulfhydryl groups of cytoplasmic components are preferentially oxidized by ozone. E. coli therefore offers a convenient model system for studying short- and long term ozone-induced cellular damage.
","abstract_html":"<p>Ozone is a major component of photochemical smog. High levels of this pollutant, sufficient to affect human health are found in many urban areas worldwide. Though limited studies in humans are supported by extensive findings from animal experiments, a difficulty in interpreting the results of these experiments has lead to an ambiguity on the biochemical mechanism of ozone toxicity. To elucidate the mechanism by which ozone causes cell damage and eventual cell death we conducted a comprehensive study using <em>Escherichia coli</em> K-12 as a model.</p> <p>Studies on the comparative inactivation of bacteriophage lambda (λ), <em>Escherichia coli</em>, and <em>Candida albicans</em> showed that λ was significantly more sensitive to ozone, in buffered solutions. The quenching effect of antioxidants in body fluids decreased the inactivation rate of λ. Short interval exposure of <em>E. coli</em> K-12 transformed with pACYC184 plasmid DNA resulted in protein and nucleic acid leakage and production of thiobarbituric acid reactive substances, without affecting cell viability. The intracellular components, protein and plasmid DNA, remained intact. The enzymes malate dehydrogenase, lactate dehydrogenase and glutathione disulfide reductase were unaffected, while glyceraldehyde-3-phosphate dehydrogenase activity decreased significantly. Glutathione and total sulfhydryl compounds were also very sensitive to ozone oxidation. With longer duration of ozone exposure cell viability decreased with a more significant increase in lipid oxidation and protein and nucleic acid leakage. The total intracellular proteins and plasmid DNA showed progressive degradation corresponding to the decrease in cell viability.</p> <p>Cell survival, induction of lipid oxidation and intracellular protein and DNA damage in two strains of <em>E. coli</em> K-12 (<em>recA</em> and wild type) were shown to be equally susceptible to ozone. Rec A protein levels decreased subsequent to ozone exposure indicating that this enzyme is not involved in the DNA repair process after ozone-induced damage. The membrane components are the primary targets of ozone damage with subsequent reactions involving the intracellular components, protein and DNA. The sulfhydryl groups of cytoplasmic components are preferentially oxidized by ozone. <em>E. coli</em> therefore offers a convenient model system for studying short- and long term ozone-induced cellular damage.</p>","abstract_has_math":false,"creators":["Komanapalli, Indira Ruth"],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":"Microbiology","degree_department":null,"school":null,"contributors":["Benjamin H. S. Lau","Robert L. Health","James D. Kettering","Subburaman Mohan","Brain J. Mudd"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1997,"date_issued":"1997-06-01T07:00:00Z","date_published":"1997-06-01T07:00:00Z","updated_at":"2026-07-24T02:54:01Z","subjects":["Amino Acids, Peptides, and Proteins","Bacteria","Bacteriology","Biological Phenomena, Cell Phenomena, and Immunity","Cellular and Molecular Physiology","Environmental Microbiology and Microbial Ecology","Enzymes and Coenzymes","Laboratory and Basic Science Research","Lipids","Microbiology","Nucleic Acids, Nucleotides, and Nucleosides","Escherichia coli -- drug effects; Escherichia coli -- cytology; Ozone -- toxicity; Bacteriophage lambda; Candida albicans -- drug effects."],"languages":["English"],"rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarsrepository.llu.edu/etd/1477","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Benjamin H. S. Lau","Robert L. Health","James D. Kettering","Subburaman Mohan","Brain J. Mudd"]},{"key":"dc:creator","label":"Author","values":["Komanapalli, Indira Ruth"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"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":["Doctor of Philosophy (PhD)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Amino Acids, Peptides, and Proteins","Bacteria","Bacteriology","Biological Phenomena, Cell Phenomena, and Immunity","Cellular and Molecular Physiology","Environmental Microbiology and Microbial Ecology","Enzymes and Coenzymes","Laboratory and Basic Science Research","Lipids","Microbiology","Nucleic Acids, Nucleotides, and Nucleosides","Escherichia coli -- drug effects; Escherichia coli -- cytology; Ozone -- toxicity; Bacteriophage lambda; Candida albicans -- drug effects."]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English"]},{"key":"dc:rights","label":"Dc Rights","values":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarsrepository.llu.edu/etd/1477"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Ozone is a major component of photochemical smog. High levels of this pollutant, sufficient to affect human health are found in many urban areas worldwide. Though limited studies in humans are supported by extensive findings from animal experiments, a difficulty in interpreting the results of these experiments has lead to an ambiguity on the biochemical mechanism of ozone toxicity. To elucidate the mechanism by which ozone causes cell damage and eventual cell death we conducted a comprehensive study using Escherichia coli K-12 as a model.
Studies on the comparative inactivation of bacteriophage lambda (λ), Escherichia coli, and Candida albicans showed that λ was significantly more sensitive to ozone, in buffered solutions. The quenching effect of antioxidants in body fluids decreased the inactivation rate of λ. Short interval exposure of E. coli K-12 transformed with pACYC184 plasmid DNA resulted in protein and nucleic acid leakage and production of thiobarbituric acid reactive substances, without affecting cell viability. The intracellular components, protein and plasmid DNA, remained intact. The enzymes malate dehydrogenase, lactate dehydrogenase and glutathione disulfide reductase were unaffected, while glyceraldehyde-3-phosphate dehydrogenase activity decreased significantly. Glutathione and total sulfhydryl compounds were also very sensitive to ozone oxidation. With longer duration of ozone exposure cell viability decreased with a more significant increase in lipid oxidation and protein and nucleic acid leakage. The total intracellular proteins and plasmid DNA showed progressive degradation corresponding to the decrease in cell viability.
Cell survival, induction of lipid oxidation and intracellular protein and DNA damage in two strains of E. coli K-12 (recA and wild type) were shown to be equally susceptible to ozone. Rec A protein levels decreased subsequent to ozone exposure indicating that this enzyme is not involved in the DNA repair process after ozone-induced damage. The membrane components are the primary targets of ozone damage with subsequent reactions involving the intracellular components, protein and DNA. The sulfhydryl groups of cytoplasmic components are preferentially oxidized by ozone. E. coli therefore offers a convenient model system for studying short- and long term ozone-induced cellular damage.
"]},{"key":"dc:title","label":"Title","values":["Cellular Responses in ESCHERICHIA COLI to Lethal and Sublethal Doses of Ozone"]}]}],"canonical_facts":{"dc:contributor":["Benjamin H. S. Lau","Robert L. Health","James D. Kettering","Subburaman Mohan","Brain J. Mudd"],"dc:creator":["Komanapalli, Indira Ruth"],"dc:description.abstract":["Ozone is a major component of photochemical smog. High levels of this pollutant, sufficient to affect human health are found in many urban areas worldwide. Though limited studies in humans are supported by extensive findings from animal experiments, a difficulty in interpreting the results of these experiments has lead to an ambiguity on the biochemical mechanism of ozone toxicity. To elucidate the mechanism by which ozone causes cell damage and eventual cell death we conducted a comprehensive study using Escherichia coli K-12 as a model.
Studies on the comparative inactivation of bacteriophage lambda (λ), Escherichia coli, and Candida albicans showed that λ was significantly more sensitive to ozone, in buffered solutions. The quenching effect of antioxidants in body fluids decreased the inactivation rate of λ. Short interval exposure of E. coli K-12 transformed with pACYC184 plasmid DNA resulted in protein and nucleic acid leakage and production of thiobarbituric acid reactive substances, without affecting cell viability. The intracellular components, protein and plasmid DNA, remained intact. The enzymes malate dehydrogenase, lactate dehydrogenase and glutathione disulfide reductase were unaffected, while glyceraldehyde-3-phosphate dehydrogenase activity decreased significantly. Glutathione and total sulfhydryl compounds were also very sensitive to ozone oxidation. With longer duration of ozone exposure cell viability decreased with a more significant increase in lipid oxidation and protein and nucleic acid leakage. The total intracellular proteins and plasmid DNA showed progressive degradation corresponding to the decrease in cell viability.
Cell survival, induction of lipid oxidation and intracellular protein and DNA damage in two strains of E. coli K-12 (recA and wild type) were shown to be equally susceptible to ozone. Rec A protein levels decreased subsequent to ozone exposure indicating that this enzyme is not involved in the DNA repair process after ozone-induced damage. The membrane components are the primary targets of ozone damage with subsequent reactions involving the intracellular components, protein and DNA. The sulfhydryl groups of cytoplasmic components are preferentially oxidized by ozone. E. coli therefore offers a convenient model system for studying short- and long term ozone-induced cellular damage.
"],"dc:identifier":["https://scholarsrepository.llu.edu/etd/1477"],"dc:language":["English"],"dc:rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"dc:subject":["Amino Acids, Peptides, and Proteins","Bacteria","Bacteriology","Biological Phenomena, Cell Phenomena, and Immunity","Cellular and Molecular Physiology","Environmental Microbiology and Microbial Ecology","Enzymes and Coenzymes","Laboratory and Basic Science Research","Lipids","Microbiology","Nucleic Acids, Nucleotides, and Nucleosides","Escherichia coli -- drug effects; Escherichia coli -- cytology; Ozone -- toxicity; Bacteriophage lambda; Candida albicans -- drug effects."],"dc:title":["Cellular Responses in ESCHERICHIA COLI to Lethal and Sublethal Doses of Ozone"],"thesis:degree_discipline":["Microbiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T02:54:01Z"}