Persistent Link:
http://hdl.handle.net/10150/278219
Title:
Vitamin E turnover in cultured pulmonary alveolar macrophages
Author:
Hoeger, Glenn Charles, 1962-
Issue Date:
1992
Publisher:
The University of Arizona.
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.
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.
Type:
text; Thesis-Reproduction (electronic)
Keywords:
Health Sciences, Toxicology.; Biology, Animal Physiology.; Health Sciences, Nutrition.
Degree Name:
M.S.
Degree Level:
masters
Degree Program:
Graduate College
Degree Grantor:
University of Arizona
Advisor:
Liebler, Daniel C.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleVitamin E turnover in cultured pulmonary alveolar macrophagesen_US
dc.creatorHoeger, Glenn Charles, 1962-en_US
dc.contributor.authorHoeger, Glenn Charles, 1962-en_US
dc.date.issued1992en_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.description.abstractVitamin 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.en_US
dc.typetexten_US
dc.typeThesis-Reproduction (electronic)en_US
dc.subjectHealth Sciences, Toxicology.en_US
dc.subjectBiology, Animal Physiology.en_US
dc.subjectHealth Sciences, Nutrition.en_US
thesis.degree.nameM.S.en_US
thesis.degree.levelmastersen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorLiebler, Daniel C.en_US
dc.identifier.proquest1350790en_US
dc.identifier.bibrecord.b25469885en_US
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