rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    non sort: The
    title: Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus
  name:
    name part: Francis Stuart, Samantha Danielle
    role:
      role term: creator
    role:
      role term: author.
  name:
    name part: Villalobos, Alice
    role:
      role term: thesis advisor.
  name:
    name part: Texas A & M University
    role:
      role term: degree granting institution.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2015
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource.
  abstract: Cadmium (Cd) is a toxic heavy metal with no known physiological function in higher order animals. Previous studies in primary cultures of neonatal rat choroid plexus (CP) epithelial cells indicated Cd induced oxidative stress and stimulated apical choline transport, and suggested zinc (Zn) supplementation might abate both oxidative stress and modulation of transport. The objective of this thesis was to elucidate how Zn, a nutritive mineral normally accumulated by CP, attenuated oxidative stress. I hypothesize that Zn, which can function as a pro-antioxidant, abates Cd-induced oxidative stress either by induction of metallothionein-1 (MT-1) or enhancement of glutathione (GSH) biochemistry. Thus, in primary cultures of neonatal rat CP epithelial cells, I characterized the effects of sub-micromolar Cd and efficacy of Zn supplementation to attenuate Cd-induced cellular and oxidative stress without or with manipulation of GSH synthesis. To characterize the Cd-induced stress response, CP epithelial cells were treated with 0 or 500 nM CdCl₂ in serum-free medium (SFM) for 12 h; samples were collected at 3, 6, 9, and 12 h. Induction of heme oxygenase-1 (HO-1), heat-shock protein 70 (HSP70), and metallothionein-1 (MT-1) in Cd-treated cells was compared to time-matched controls by immunoblot and qRT-PCR analyses. Cd induced the catalytic and modifier subunits of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis. To elucidate the effects Zn supplementation in Cd-treated cells depleted of GSH, cells were supplemented for 48 h with 0 or 25 [mu]M ZnCl₂ alone or with 100 [mu]M buthionine sulfoximine (BSO), an inhibitor of GCL, before treatment with 0 or 500 nM CdCl₂ ± 100 [mu]M BSO ± 10[mu]M ZnCl₂ in SFM for 12 h. By luminescence assay, intracellular GSH and oxidized glutathione (GSSG) concentrations were measured. Cd increased intracellular GSH and GSSG, but markedly decreased GSH:GSSG ratio. Inhibition of GSH synthesis exacerbated Cd-induced stress. Howev…
  note: by Samantha Danielle Francis Stuart.
  note: "Major Subject: Toxicology"
  note: Includes vita.
  note: Master of Science Texas A & M University 2014 http://hdl.handle.net/1969.1/152822
  note: Includes bibliographical references.
  note: Text (Thesis)
  subject:
    topic: Major Toxicology
  subject:
    topic: Choroid plexus
  subject:
    topic: Cadmium
  subject:
    topic: Zinc
  subject:
    topic: Oxidative stress
  subject:
    topic: Glutathione
  subject:
    topic: Metallothionein
  subject:
    topic: Heat-shock protein 70
  subject:
    topic: Hemeoxygenase
  identifier: http://hdl.handle.net/1969.1/152822
  record info:
    record content source: TXA
    record creation date: 150211
    record change date: 20151206125945.0
    record identifier: in00003432039
    language of cataloging:
      language term: eng