Ca^(2+) Movement Induced by Deltamethrin in PC3 Human Prostate Cancer Cells

This study explored the effect of deltamethrin, a pesticide, on intracellular free Ca^(2+) concentration ([Ca^(2+)]i) in PC3 human prostate cancer cells. Deltamethrin at concentrations between 5 μM and 20 μM evoked [Ca^(2+)]i rises in a concentration-dependent manner. This Ca^(2+) signal was inhibited by 22% by removal of extracellular Ca^(2+). Nifedipine, econazole, and SKF96365 also inhibited the Ca^(2+) signal. Treatment with the endoplasmic reticulum Ca^(2+) pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) in Ca^(2+)-free medium nearly abolished deltamethrin-induced [Ca^(2+)]i rises. Treatment with deltamethrin also inhibited most of BHQ-induced [Ca^(2+)]i rises. Inhibition of phospholipase C (PLC) with U73122 failed to alter deltamethrin-evoked [Ca^(2+)]i rises. Deltamethrin killed cells at concentrations of 20-100 μM in a concentration-dependent fashion. Chelation of cytosolic Ca^(2+) with 1,2-bis (2-aminophenoxy) ethane-N, N, N', N'-tetraacetic acid/acetoxymethyl ester (BAPTA/AM) did not prevent deltamethrin's cytotoxicity. Together, in PC3 human prostate cancer cells, deltamethrin induced [Ca^(2+)]i rises that involved Ca^(2+) entry through store-operated Ca^(2+) channels and PLC-independent Ca^(2+) release from the endoplasmic reticulum. Deltamethrin induced cytotoxicity in a Ca^(2+)-independent manner.