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Abstract
AbstractThe effect of the antidepressant paroxetine on cytosolic free Ca2+ concentrations ([Ca2+]i) in PC3 human prostate cancer cells is unclear. This study explored whether paroxetine changed basal [Ca2+]i levels in suspended PC3 cells by using fura‐2 as a Ca2+‐sensitive fluorescent dye. Paroxetine at concentrations between 10–150 µM increased [Ca2+]i in a concentration‐dependent manner. The Ca2+ signal was reduced by 55% by removing extracellular Ca2+. Paroxetine‐induced Ca2+ influx was inhibited by the store‐operated Ca2+ channel blockers econazole and SK&F96365, the phospholipase A2 inhibitor aristolochic acid, and protein kinase C modulators. In Ca2+‐free medium, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitors thapsigargin, 2,5‐di‐tert‐butylhydroquinone (BHQ), or cyclopiazonic acid (CPA) all abolished paroxetine‐induced [Ca2+]i rise. Inhibition of phospholipase C with U73122 inhibited paroxetine‐induced [Ca2+]i rise by 80%. Collectively, in PC3 cells, paroxetine induced [Ca2+]i rise by causing phospholipase C‐dependent 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. Drug Dev Res, 2009. © 2009 Wiley‐Liss, Inc.
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