Title page for etd-0716112-164621


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URN etd-0716112-164621
Author Wei-Chuan Liao
Author's Email Address No Public.
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Department Biological Sciences
Year 2011
Semester 2
Degree Ph.D.
Type of Document
Language English
Title Effect of thimerosal on Ca2+ movement and apoptosis in PC3 prostate cancer cells
Date of Defense 2011-06-20
Page Count 109
Keyword
  • PC3 cells
  • Ca2+
  • thimerosal
  • Abstract Thimerosal is a mercury-containing component found in many vaccine preparations and used as a preservative. It causes Ca2+ movement across cell membrane in different cells that may be mediated via effects on different receptors and ion channels.
    A rise in intracellular free Ca2+ concentrations ([Ca2+]i) is a key signal for many pathophysiological processes in cells, including apoptosis and necrosis. Thimerosal increases [Ca2+]i in different cell types. The mechanisms underlying thimerosal-induced Ca2+ signal vary with cell types.
    The present study evaluated the effects of thimerosal on [Ca2+]i in human prostate cancer cells (PC3). WST-1 reduction assays and propidium iodide-staining assays were used to determine cell viability and apoptosis in the presence of thimerosal. The experimental results may be helpful to understand the pahrmocological and toxicological effects of thimerosal on cells from important organs.
    Results showed that thimerosal (10–200μM) increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. Thimerosal-induced Ca2+ influx was inhibited by econazole, SKF963656, the phospholipase A2 inhibitor aristolochic acid, and protein kinase C modulators [phorbol 12-myristate 13-acetate (PMA) and GF109203X]. In Ca2+-free medium, a 200-mM thimerosal-induced [Ca2+]i rise was partly inhibited after pretreatment with 2,5-di-tert-butylhydroquinone (BHQ) (an endoplasmic reticulum Ca2+ pump inhibitor). Thimerosal at 1–7μM induced cell death in a concentration-dependent manner that was not reversed when cytosolic Ca2+ was chelated with 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid (BAPTA). Propidium iodide staining suggests that apoptosis played a role in the death.
    Collectively, in PC3 cells, thimerosal induced [Ca2+]i rise by causing Ca2+ release from the endoplasmic reticulum and Ca2+ influx via store-operated Ca2+ channels in a manner regulated by protein kinase C and phospholipase A2. Thimerosal also induced cell death in a Ca2+-independent apoptotic manner.
    Advisory Committee
  • Chen-Chih Kao - chair
  • none - co-chair
  • none - co-chair
  • Chung-Ren Jan - advisor
  • Chen-Fu Shaw - advisor
  • Files
  • etd-0716112-164621.pdf
  • Indicate in-campus at 1 year and off-campus access at 1 year.
    Date of Submission 2012-07-16

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