{"id":{"repo_id":"vt","oai_identifier":"oai:vtechworks.lib.vt.edu:10919/41443"},"canonical_url":"https://search.dev.ndltd.org/etd/vt/oai:vtechworks.lib.vt.edu:10919/41443","repository":{"repo_id":"vt","name":"Virginia Tech","base_url":"https://vtechworks.lib.vt.edu/oai/request"},"display":{"title":"Utilization of mitochondrial and microsomal metabolism for the assessment of toxicity","abstract":"Short-term toxicity tests utilizing mitochondrial and microsomal metabolism were developed and applied to a series of eight quinones. In the mitochondrial assay, the degree to which test compounds inhibited mitochondrial respiration varied from an EC50 of 9 μM to l25 μM. In the microsomal assay, the maximum percent increase over control oxygen consumption rates elicited by the quinones ranged from eight percent to 837 percent. The ability of the compounds to stimulate microsomal oxygen uptake reflects their capability to redox cycle and form reactive oxygen species. Experiments were conducted to evaluate the relationship between the rate of quinone redox cycling and the extent of microsomal lipid peroxidation, a possible toxic insult associated with reactive oxygen species. Results of the mitochondrial and microsomal assays were statistically correlated with several quinone physicochemical parameters and qualitatively compared to reduction potential. The biological response observed in both test systems appeared to be most strongly influenced by the reduction potential of the quinone and biomechanisms of action were suggested based on this relationship. To assess the ability of the mitochondrial and microsomal assays to indicate toxicity of the quinonoid compounds, results were statistically correlated with literature-derived toxicity data. It was concluded that the mitochondrial assay appears to be a valid indicator of acute toxicity, while the microsomal assay better portends the potential for chronic toxicity.","abstract_html":"Short-term toxicity tests utilizing mitochondrial and microsomal metabolism were developed and applied to a series of eight quinones. In the mitochondrial assay, the degree to which test compounds inhibited mitochondrial respiration varied from an EC50 of 9 μM to l25 μM. In the microsomal assay, the maximum percent increase over control oxygen consumption rates elicited by the quinones ranged from eight percent to 837 percent. The ability of the compounds to stimulate microsomal oxygen uptake reflects their capability to redox cycle and form reactive oxygen species. Experiments were conducted to evaluate the relationship between the rate of quinone redox cycling and the extent of microsomal lipid peroxidation, a possible toxic insult associated with reactive oxygen species. Results of the mitochondrial and microsomal assays were statistically correlated with several quinone physicochemical parameters and qualitatively compared to reduction potential. The biological response observed in both test systems appeared to be most strongly influenced by the reduction potential of the quinone and biomechanisms of action were suggested based on this relationship. To assess the ability of the mitochondrial and microsomal assays to indicate toxicity of the quinonoid compounds, results were statistically correlated with literature-derived toxicity data. It was concluded that the mitochondrial assay appears to be a valid indicator of acute toxicity, while the microsomal assay better portends the potential for chronic toxicity.","abstract_has_math":false,"creators":["Bramble, Lisa Anne"],"institution":"Virginia Tech","degree_name":"Master of Science","degree_level":"masters","degree_discipline":"Environmental Sciences and Engineering","degree_department":"Environmental Sciences and Engineering","school":null,"contributors":[],"advisors":[],"committee_chairs":["Boardman, Gregory D."],"committee_members":["Bevan, David R.","Dietrich, Andrea M."],"year":1990,"date_issued":"1990-01-18","date_published":"1990-01-18","updated_at":"2026-07-22T22:20:05Z","subjects":[],"languages":["en"],"rights":["In Copyright"],"rights_urls":["http://rightsstatements.org/vocab/InC/1.0/"],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-03122009-040409"],"render_values":[{"text":"etd-03122009-040409","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/10919/41443","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.committeechair","label":"Committee Chair","values":["Boardman, Gregory D."]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Bevan, David R.","Dietrich, Andrea M."]},{"key":"dc:contributor.department","label":"Department","values":["Environmental Sciences and Engineering"]},{"key":"dc:creator","label":"Author","values":["Bramble, Lisa Anne"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2014-03-14T21:31:03Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2014-03-14T21:31:03Z","2009-03-12"]},{"key":"dc:date.issued","label":"Date","values":["1990-01-18"]},{"key":"dc:publisher","label":"Institution","values":["Virginia Tech"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"dc:type.dcmitype","label":"Dc Type Dcmitype","values":["Text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Environmental Sciences and Engineering"]},{"key":"thesis:degree_level","label":"Degree Level","values":["masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["Virginia Polytechnic Institute and State University"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["In Copyright"]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://rightsstatements.org/vocab/InC/1.0/"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-03122009-040409"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10919/41443"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Short-term toxicity tests utilizing mitochondrial and microsomal metabolism were developed and applied to a series of eight quinones. In the mitochondrial assay, the degree to which test compounds inhibited mitochondrial respiration varied from an EC50 of 9 μM to l25 μM. In the microsomal assay, the maximum percent increase over control oxygen consumption rates elicited by the quinones ranged from eight percent to 837 percent. The ability of the compounds to stimulate microsomal oxygen uptake reflects their capability to redox cycle and form reactive oxygen species. Experiments were conducted to evaluate the relationship between the rate of quinone redox cycling and the extent of microsomal lipid peroxidation, a possible toxic insult associated with reactive oxygen species. Results of the mitochondrial and microsomal assays were statistically correlated with several quinone physicochemical parameters and qualitatively compared to reduction potential. The biological response observed in both test systems appeared to be most strongly influenced by the reduction potential of the quinone and biomechanisms of action were suggested based on this relationship. To assess the ability of the mitochondrial and microsomal assays to indicate toxicity of the quinonoid compounds, results were statistically correlated with literature-derived toxicity data. 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The biological response observed in both test systems appeared to be most strongly influenced by the reduction potential of the quinone and biomechanisms of action were suggested based on this relationship. To assess the ability of the mitochondrial and microsomal assays to indicate toxicity of the quinonoid compounds, results were statistically correlated with literature-derived toxicity data. 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