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dc.contributor.advisorWatson, Ronald Rossen_US
dc.contributor.authorZhang, Jin
dc.creatorZhang, Jinen_US
dc.date.accessioned2013-04-11T08:46:08Z
dc.date.available2013-04-11T08:46:08Z
dc.date.issued2002en_US
dc.identifier.urihttp://hdl.handle.net/10150/280048
dc.description.abstractEnvironmental tobacco smoke (ETS) is a complex mixture of chemicals generated during the burning of tobacco products. The principle contributor to ETS is side-stream cigarette smoke (SSCS), the material emitted from the smoldering tobacco product between puffs Our hypothesis is that reactive oxygen species from SSCS are playing an essential role in disease promotion and antioxidant supplementation (a single form of alpha-tocopherol or a mixture of multiple antioxidants) will potentially prevent SSCS associated tissue damage, pulmonary dysfunction. The specific aims of the present study are to determine if: (1) SSCS would induce tissue lipid peroxidation and proinflammatory responses; (2) SSCS would provoke pulmonary and cardiac function changes; (3) SSCS would cause oxidative stress, reduce nutrient concentrations and suppress immune function in murine retrovirus infections; (4) dietary alpha-tocopherol, specifically, can enhance resistance to oxidative damage by SSCS and improve lung function; (5) multiple antioxidant supplementation can modulate proinflammatory cytokine secretion and tissue lipid peroxidation induced by SSCS exposure in old healthy mice. SSCS exposure methodology in a murine model was developed to facilitate these goals. For the first time we established a SSCS model in murine retrovirus infection. Also we conduced a SSCS dose-response model for a cardiac function study. We found that SSCS exposure in mice consistently increased oxidation, depleted tissue vitamin E levels, and promoted inflammatory cytokines production. SSCS exposure at 120-min/day, 5 days/week for 12 weeks decreased heart contractile function and increased vascular resistance. SSCS induced increased oxidative stress, reduced nutrient concentrations and suppressed immune function, which could make mice with murine retrovirus more susceptible to opportunistic infections. Dietary alpha-tocopherol enhanced resistance against SSCS-induced oxidation and improved lung function, primarily through the antioxidant property of alpha-tocopherol and its modulation of local cytokine production. The multiple antioxidant with beta-carotene, bioflavanoids, Coenzyme Q10, d-alpha-tocopherol, L-ascorbic acid, L-carnitine, magnesium, N-acetylcysteine, retinol, selenium and zinc given as a dietary supplementation prevented oxidation and IL-6 production in healthy old mice during SSCS exposure. (Abstract shortened by UMI.)
dc.language.isoen_USen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectHealth Sciences, Toxicology.en_US
dc.subjectHealth Sciences, Nutrition.en_US
dc.subjectHealth Sciences, Public Health.en_US
dc.subjectHealth Sciences, Immunology.en_US
dc.titleImmunological modulation of antioxidants in side-stream cigarette smoke (SSCS) exposed miceen_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.identifier.proquest3053916en_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineNutritional Sciencesen_US
thesis.degree.namePh.D.en_US
dc.identifier.bibrecord.b42830680en_US
refterms.dateFOA2018-05-25T10:18:55Z
html.description.abstractEnvironmental tobacco smoke (ETS) is a complex mixture of chemicals generated during the burning of tobacco products. The principle contributor to ETS is side-stream cigarette smoke (SSCS), the material emitted from the smoldering tobacco product between puffs Our hypothesis is that reactive oxygen species from SSCS are playing an essential role in disease promotion and antioxidant supplementation (a single form of alpha-tocopherol or a mixture of multiple antioxidants) will potentially prevent SSCS associated tissue damage, pulmonary dysfunction. The specific aims of the present study are to determine if: (1) SSCS would induce tissue lipid peroxidation and proinflammatory responses; (2) SSCS would provoke pulmonary and cardiac function changes; (3) SSCS would cause oxidative stress, reduce nutrient concentrations and suppress immune function in murine retrovirus infections; (4) dietary alpha-tocopherol, specifically, can enhance resistance to oxidative damage by SSCS and improve lung function; (5) multiple antioxidant supplementation can modulate proinflammatory cytokine secretion and tissue lipid peroxidation induced by SSCS exposure in old healthy mice. SSCS exposure methodology in a murine model was developed to facilitate these goals. For the first time we established a SSCS model in murine retrovirus infection. Also we conduced a SSCS dose-response model for a cardiac function study. We found that SSCS exposure in mice consistently increased oxidation, depleted tissue vitamin E levels, and promoted inflammatory cytokines production. SSCS exposure at 120-min/day, 5 days/week for 12 weeks decreased heart contractile function and increased vascular resistance. SSCS induced increased oxidative stress, reduced nutrient concentrations and suppressed immune function, which could make mice with murine retrovirus more susceptible to opportunistic infections. Dietary alpha-tocopherol enhanced resistance against SSCS-induced oxidation and improved lung function, primarily through the antioxidant property of alpha-tocopherol and its modulation of local cytokine production. The multiple antioxidant with beta-carotene, bioflavanoids, Coenzyme Q10, d-alpha-tocopherol, L-ascorbic acid, L-carnitine, magnesium, N-acetylcysteine, retinol, selenium and zinc given as a dietary supplementation prevented oxidation and IL-6 production in healthy old mice during SSCS exposure. (Abstract shortened by UMI.)


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