These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Effect of fluoxetine on [Ca²⁺]i and cell viability in OC2 human oral cancer cells.
    Author: Lin KL, Chou CT, Cheng JS, Chang HT, Liang WZ, Kuo CC, Chen IL, Tseng LL, Shieh P, Wu RF, Kuo DH, Jan CR.
    Journal: Chin J Physiol; 2014 Oct 31; 57(5):256-64. PubMed ID: 25241985.
    Abstract:
    Fluoxetine is a serotonin-specific reuptake inhibitor that has been used as an antidepressant. This study examined the effect of fluoxetine on cytosolic free Ca²⁺ concentrations ([Ca2⁺]i) and viability in OC2 human oral cancer cells. The Ca²⁺-sensitive fluorescent dye fura-2 was used to measure [Ca²⁺]i, and the water soluble tetrazolium (WST-1) regent was used to measure viability. Fluoxetine induced [Ca²⁺]i rises concentration-dependently. The response was reduced by half by removing extracellular Ca²⁺. Fluoxetine-induced Ca²⁺ entry was enhanced by activation of protein kinase C (PKC) with phorbol 12-myristate 13 acetate (PMA) but was inhibited by inhibition of the enzyme with GF109203X. In Ca²⁺-free medium, treatment with the endoplasmic reticulum Ca²⁺ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) or thapsigargin abolished fluoxetine-evoked [Ca²⁺]i rise. Conversely, treatment with fluoxetine inhibited BHQ/thapsigargin-evoked [Ca²⁺]i rise. Inhibition of phospholipase C (PLC) with U73122 abolished fluoxetine-induced [Ca²⁺]i rise. At 20-80 μM, fluoxetine decreased cell viability concentration-dependently, which was not altered by chelating cytosolic Ca²⁺ with 1,2-bis(2- aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). At 20-60 μM, fluoxetine induced apoptosis as detected by annexin V/propidium iodide (PI) staining. Together, in OC2 cells, fluoxetine induced [Ca²⁺]i rises by evoking PLC-dependent Ca²⁺ release from the endoplasmic reticulum and Ca²⁺ entry via PKC-regulated mechanisms. Fluoxetine also caused Ca²⁺-independent apoptosis.
    [Abstract] [Full Text] [Related] [New Search]