KUKU

KU ScholarWorks

  • myKU
  • Email
  • Enroll & Pay
  • KU Directory
    • Login
    View Item 
    •   KU ScholarWorks
    • Dissertations and Theses
    • Theses
    • View Item
    •   KU ScholarWorks
    • Dissertations and Theses
    • Theses
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Mechanistic Studies on Arsenic Toxicity in Endothelial Cells

    Thumbnail
    View/Open
    Available after: 2020-08-31 (1.452Mb)
    Issue Date
    2018-08-31
    Author
    Chen, Jiani
    Publisher
    University of Kansas
    Format
    90 pages
    Type
    Thesis
    Degree Level
    M.S.
    Discipline
    Pharmacology & Toxicology
    Rights
    Copyright held by the author.
    Metadata
    Show full item record
    Abstract
    Arsenic is a well-established human toxin. Over 200 million people worldwide are exposed to arsenic, mainly through drinking water. Recently, several epidemiological studies have reported that even low concentrations of arsenic impair neurological functions across a broad age range in human [1]. However, the cellular and molecular mechanisms of arsenic’s effect on the central nervous system (CNS) are not well understood. The blood-brain barrier (BBB) is a complex multicellular structure separating the CNS from the systemic circulation and protects the neural tissue from toxins and pathogens. Alterations in the BBB are an important component of pathology in many neurological disorders [2]. Therefore, arsenic may have a toxic impact on the BBB and thus affect the function of CNS. Since brain endothelial cells (BECs) are the major component of the BBB and play important roles in maintaining the functional integrity of brain tissue under toxic exposure, we focused on arsenic-induced alterations in BECs in our study. Previously, our laboratory has reported that reactive oxygen species (ROS) play an important role in an arsenic-induced increase in brain endothelial cell permeability[3]. However, the underlying mechanism of arsenic-induced ROS generation in endothelial cells and how ROS regulate endothelial cell functions are unclear. Mitochondria are considered as the major source of ROS generation in mammalian cells and arsenic-induced mitochondrial dysfunction has been reported in many studies, which suggest that it may be associated with arsenic-induced oxidative stress in endothelial cells (ECs). In addition, autophagy, which is regulated by oxidative stress, plays an important role to control endothelial permeability and maintain redox balance in ECs and it may also be involved in arsenic toxicity in BECs [4].
    URI
    http://hdl.handle.net/1808/27829
    Collections
    • Pharmacy Dissertations and Theses [118]
    • Theses [3901]

    Items in KU ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.


    We want to hear from you! Please share your stories about how Open Access to this item benefits YOU.


    Contact KU ScholarWorks
    785-864-8983
    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    Image Credits
     

     

    Browse

    All of KU ScholarWorksCommunities & CollectionsThis Collection

    My Account

    Login

    Statistics

    View Usage Statistics

    Contact KU ScholarWorks
    785-864-8983
    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    Image Credits
     

     

    The University of Kansas
      Contact KU ScholarWorks
    Lawrence, KS | Maps
     
    • Academics
    • Admission
    • Alumni
    • Athletics
    • Campuses
    • Giving
    • Jobs

    The University of Kansas prohibits discrimination on the basis of race, color, ethnicity, religion, sex, national origin, age, ancestry, disability, status as a veteran, sexual orientation, marital status, parental status, gender identity, gender expression and genetic information in the University’s programs and activities. The following person has been designated to handle inquiries regarding the non-discrimination policies: Director of the Office of Institutional Opportunity and Access, IOA@ku.edu, 1246 W. Campus Road, Room 153A, Lawrence, KS, 66045, (785)864-6414, 711 TTY.

     Contact KU
    Lawrence, KS | Maps