In:
The Kaohsiung Journal of Medical Sciences, Wiley, Vol. 31, No. 1 ( 2015-01), p. 1-8
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
1607-551X
,
2410-8650
DOI:
10.1016/j.kjms.2014.10.009
Language:
English
Publisher:
Wiley
Publication Date:
2015
detail.hit.zdb_id:
2202782-8
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