In:
Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 104, No. 5 ( 2009-05), p. 345-351
Abstract:
Abstract: Cadmium (Cd 2+ ) is an industrial and environmental metal. The effect of Cd 2+ on intracellular free‐Ca 2+ levels ([Ca 2+ ] i ) and viability in Madin Darby canine kidney cells was explored. Cd 2+ increased [Ca 2+ ] i in a concentration‐dependent manner with an EC 50 of 85 µM. Cd 2+ ‐induced Mn 2+ entry demonstrated Ca 2+ influx. Removal of extracellular Ca 2+ decreased the [Ca 2+ ] i signal by 60%. The [Ca 2+ ] i signal was inhibited by La 3+ but not by L‐type Ca 2+ channel blockers. In Ca 2+ ‐free medium, Cd 2+ ‐induced [Ca 2+ ] i signal was abolished by pre‐treatment with 1 µM thapsigargin (an endoplasmic reticulum Ca 2+ pump inhibitor) and 2 µM carbonylcyanide m‐chlorophenylhydrazone (CCCP; a mitochondrial uncoupler). Cd 2+ ‐induced Ca 2+ release was not altered by inhibition of phospholipase C. At concentrations between 10 and 100 µM, Cd 2+ killed cells in a concentration‐dependent manner. The cytotoxic effect of 100 µM Cd 2+ was reversed by pre‐chelating cytosolic Ca 2+ with BAPTA. Cd 2+ ‐induced apoptosis was demonstrated by propidium iodide. Collectively, this study shows that Cd 2+ induced a [Ca 2+ ] i increase in Madin Darby canine kidney cells via evoking Ca 2+ entry through non‐selective Ca 2+ channels, and releasing stored Ca 2+ from endoplasmic reticulum and mitochondria in a phospholipase C‐independent manner.
Type of Medium:
Online Resource
ISSN:
1742-7835
,
1742-7843
DOI:
10.1111/pto.2009.104.issue-5
DOI:
10.1111/j.1742-7843.2009.00391.x
Language:
English
Publisher:
Wiley
Publication Date:
2009
detail.hit.zdb_id:
2151592-X
SSG:
15,3
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