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:
    title: Cytotoxicological response to engineered nanomaterials
    sub title: a pathway-driven process
  name:
    name part: Romoser, Amelia Antonia.
    role:
      role term: creator
  name:
    name part: Criscitiello, Michael F.
    role:
      role term: thesis advisor.
  name:
    name part: Sayes, Christie M.
    role:
      role term: thesis advisor.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2012
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource.
  abstract: Nanoparticles, while included in a growing number of consumer products, may pose risks to human health due to heavy metal leaching and/or the production of reactive oxygen species following exposures. Subcellular mechanisms of action triggered as a result of exposure to various nanoparticles are still largely unexplored. In this work, an effort to elucidate such toxicological parameters was accomplished by evaluating oxidative stress generation, changes in gene and protein expression, and cell cycle status after low-dose exposures to a variety of metal and carbon-based nanomaterials in primary human dermal cells. Additionally, mitigation of nanoparticle toxicity via microencapsulation was investigated to assess the feasibility of utilizing nanomaterials in dermally implantable biosensor applications. Cellular immune and inflammatory processes were measured via qPCR and immunoblotting, which revealed gene and protein expression modulation along the NF-[kappa]B pathway after a variety of nanoparticle exposures. The role of immunoregulatory transcription factor NF-[kappa]B was examined in an oxidative stress context in cells exposed to a panel of nanoparticles, whereby glutathione conversion and modulation of oxidative stress proteins in normal and NF-[kappa]B knockdown human dermal fibroblasts were monitored. Results revealed decreased antioxidant response and corresponding increased levels of oxidative stress and cell death in exposed normal cells, compared to NF-[kappa]B incompetent cells. However, reactive oxygen species production was not an absolute precursor to DNA damage, which was measured by the comet assay, [gamma]-H2AX expression, and flow cytometry. Protein analysis revealed that map kinase p38, rather than p53, was involved in the halting of the cell cycle in S-phase after ZnO exposures, which caused DNA double strand breaks. Microencapsulation of fluorescent quantum dot nanoparticles, specifically, was utilized as a method to improve system functionality…
  note: by Amelia Antonia Romoser.
  note: "Major Subject: Toxicology"
  note: Electronic resource.
  note: Doctor of Philosophy Texas A&M University 2012 http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-10877
  note: Includes bibliographical references.
  note: Text (Dissertation)
  subject:
    topic: Major Toxicology
  subject:
    topic: ROS
  subject:
    topic: fullerol
  subject:
    topic: nanoparticles
  subject:
    topic: oxidative stress
  subject:
    topic: NF-kB
  subject:
    topic: metal oxide
  subject:
    topic: inflammatory response
  subject:
    topic: immunomodulation
  subject:
    topic: DNA damage
  subject:
    topic: microencapsulation
  subject:
    topic: quantum dot
  identifier: http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-10877
  record info:
    record content source: TXA
    record creation date: 120809
    record change date: 20150922105950.0
    record identifier: in00002771182