Vitamin E turnover in cultured pulmonary alveolar macrophages
| dc.contributor.advisor | Liebler, Daniel C. | en_US |
| dc.contributor.author | Hoeger, Glenn Charles, 1962- | |
| dc.creator | Hoeger, Glenn Charles, 1962- | en_US |
| dc.date.accessioned | 2013-04-03T13:16:53Z | |
| dc.date.available | 2013-04-03T13:16:53Z | |
| dc.date.issued | 1992 | en_US |
| dc.identifier.uri | http://hdl.handle.net/10150/278219 | |
| dc.description.abstract | Vitamin E (α-TH), the primary lipid soluble antioxidant, can protect tissues from oxidative insult. Oxidant-producing pulmonary alveolar macrophages (PAM), may depend on α-TH to prevent oxidative damage. α-TH levels in cultured PAM declined rapidly during the first 12-18 hours in culture. Approximately 60% of the decrease was detected as unoxidized alpha-TH released to RPMI 1640 (containing 5% fetal bovine serum (FBS)) culture medium. α-TH was not detected in serum-free Ham's F12 medium. PAM appeared to reabsorb α-TH from the medium. PAM activation with phorbol myristate acetate (PMA) did not affect cellular α-TH depletion. However, the amount of α-TH detected in the medium of PMA treated cultures was only 50% of that detected in medium from untreated controls. Inhibition of superoxide production with iodoacetate had no effect on cellular depletion kinetics, however medium α-TH levels were still 50% of controls. Inhibition of nitric oxide, synthesis appeared to have no effect on α-TH status. | |
| dc.language.iso | en_US | en_US |
| dc.publisher | The University of Arizona. | en_US |
| dc.rights | Copyright © 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.subject | Health Sciences, Toxicology. | en_US |
| dc.subject | Biology, Animal Physiology. | en_US |
| dc.subject | Health Sciences, Nutrition. | en_US |
| dc.title | Vitamin E turnover in cultured pulmonary alveolar macrophages | en_US |
| dc.type | text | en_US |
| dc.type | Thesis-Reproduction (electronic) | en_US |
| thesis.degree.grantor | University of Arizona | en_US |
| thesis.degree.level | masters | en_US |
| dc.identifier.proquest | 1350790 | en_US |
| thesis.degree.discipline | Graduate College | en_US |
| thesis.degree.name | M.S. | en_US |
| dc.identifier.bibrecord | .b25469885 | en_US |
| refterms.dateFOA | 2018-08-27T13:34:07Z | |
| html.description.abstract | Vitamin E (α-TH), the primary lipid soluble antioxidant, can protect tissues from oxidative insult. Oxidant-producing pulmonary alveolar macrophages (PAM), may depend on α-TH to prevent oxidative damage. α-TH levels in cultured PAM declined rapidly during the first 12-18 hours in culture. Approximately 60% of the decrease was detected as unoxidized alpha-TH released to RPMI 1640 (containing 5% fetal bovine serum (FBS)) culture medium. α-TH was not detected in serum-free Ham's F12 medium. PAM appeared to reabsorb α-TH from the medium. PAM activation with phorbol myristate acetate (PMA) did not affect cellular α-TH depletion. However, the amount of α-TH detected in the medium of PMA treated cultures was only 50% of that detected in medium from untreated controls. Inhibition of superoxide production with iodoacetate had no effect on cellular depletion kinetics, however medium α-TH levels were still 50% of controls. Inhibition of nitric oxide, synthesis appeared to have no effect on α-TH status. |
