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

Hai-Hsiang Lee ； Chiang-Ting Chou ； Wei-Zhe Liang ； Wei-Chuan Chen ； Jue-Long Wang ； Jeng-Hsien Yeh ； Chun-Chi Kuo ； Pochuen Shieh ； Daih-Huang Kuo ； Fu-An Chen ； Chung-Ren Jan

《The Chinese Journal of Physiology》 預刊文章 Pp. 1-8

https://doi.org/10.4077/CJP.2016.BAE386

並列摘要

This study explored the effect of deltamethrin, a pesticide, on [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 concentrationdependent 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 deltamethrininduced [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/AM (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.

並列關鍵字

Ca^(2+) ； deltamethrin ； endoplasmic reticulum ； phospholipase C ； prostate cancer cells ； storeoperated Ca^(2+) channels