Abstract.
The effect of the phospholipase A2 inhibitor palmitoyl trifluoromethyl ketone (PACOCF3) on Ca2+ signaling in Madin Darby canine kidney (MDCK) cells was examined using fura-2 as the fluorescent Ca2+ indicator. At a concentration of 20 µM, PACOCF3 did not change basal cytosolic free calcium concentrations ([Ca2+]i), but at concentrations of 50–250 µM PACOCF3 induced an increase in [Ca2+]i by activating extracellular Ca2+ entry which was partly suppressed by 50 µM La3+. The effect of PACOCF3 was abolished by removal of extracellular Ca2+. PACOCF3 (10 µM) enhanced both the peak value and the area under the curve of the [Ca2+]i increase induced by 10 µM ATP and 1 µM bradykinin by potentiating extracellular Ca2+ influx without affecting internal Ca2+ release. Several other phospholipase A2 inhibitors had no effect on basal [Ca2+]i or agonist-induced [Ca2+]i increases. Collectively, the results suggest that PACOCF3 alters Ca2+ signaling in renal tubular cells in a manner independent of phospholipase A2 inhibition.
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Jan, CR., Chou, KJ., Lee, K. et al. Dual action of palmitoyl trifluoromethyl ketone (PACOCF3) on Ca2+ signaling: activation of extracellular Ca2+ influx and alteration of ATP- and bradykinin-induced Ca2+ responses in Madin Darby canine kidney cells. Arch Toxicol 74, 447–451 (2000). https://doi.org/10.1007/s002040000130
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DOI: https://doi.org/10.1007/s002040000130