Open AccessCa 2+ movement and apoptosis induced by deltamethrin in Madin–Darby canine kidney canine renal tubular cells
Author(s) -
Liu FangJin,
Chou ChiangTing,
Cheng Jin Shiung,
Chang HongTai,
Liang WeiZhe,
Kuo ChunChi,
Kuo SoongYu,
Kuo DaihHuang,
Shieh Pochuen,
Chang FangRong,
Jan ChungRen
Publication year - 2015
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2014.10.009
Subject(s) - deltamethrin , endoplasmic reticulum , apoptosis , medicine , propidium iodide , microbiology and biotechnology , phospholipase c , phorbol , kidney , endocrinology , programmed cell death , protein kinase c , biology , biochemistry , kinase , receptor , pesticide , agronomy
This study explored the effect of deltamethrin, a pesticide, on free Ca 2+ concentration [Ca 2+ ] i , viability, and apoptosis in Madin–Darby canine kidney (MDCK) canine renal tubular cells. Deltamethrin at concentrations between 10μM and 40μM evoked [Ca 2+ ] i rises in a concentration‐dependent manner. The Ca 2+ entry was inhibited by nifedipine, econazole, phorbol 12‐myristate 13‐acetate, and SKF96365. Treatment with the endoplasmic reticulum Ca 2+ pump inhibitor 2,5‐di‐tert‐butylhydroquinone (BHQ) in a Ca 2+ ‐free medium abolished deltamethrin‐induced [Ca 2+ ] i rise. Treatment with deltamethrin also abolished BHQ‐induced [Ca 2+ ] i rise. Inhibition of phospholipase C (PLC) activity with U73122 abolished deltamethrin‐evoked [Ca 2+ ] i rise. Deltamethrin killed cells at 30–60μM in a concentration‐dependent manner. The cytotoxic effect of deltamethrin was not reversed by prechelating cytosolic Ca 2+ with the acetoxymethyl ester of 1,2‐bis(2‐aminophenoxy)ethane‐ N , N , N ′, N ′‐tetraacetic acid. Annexin V/propidium iodide staining data suggest that 30–50μM deltamethrin induced apoptosis. Together, in MDCK renal tubular cells, deltamethrin induced [Ca 2+ ] i rises that involved Ca 2+ entry through protein kinase C‐mediated store‐operated Ca 2+ channels, and PLC‐dependent Ca 2+ release from the endoplasmic reticulum. Deltamethrin also induced Ca 2+ ‐independent cell death that might involve apoptosis.