Unbound MEDLINE

The Garlic Ingredient Diallyl Sulfide Induces Ca(2+) Mobilization in Madin-Darby Canine Kidney Cells. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association [Food Chem Toxicol] Journal article

 
TitleThe Garlic Ingredient Diallyl Sulfide Induces Ca(2+) Mobilization in Madin-Darby Canine Kidney Cells.
Author(s)Chen CH, Su SJ, Chang KL, Huang MW, Kuo SY 
InstitutionGraduate Institute of Biomedical and Biopharmaceutical Sciences, College of Life Sciences, National Chiayi University, Chiayi 60004, Taiwan.
SourceFood Chem Toxicol 2009 Jun 22.
AbstractDiallyl sulfide (DAS), one of the major organosulfur compounds (OSCs) of garlic, is recognized as a group of potential chemoproventive compounds. In this study, we examines the early signaling effects of DAS on renal cells loaded with Ca(2+)-sensitive dye fura-2. It was found that DAS caused an immediate and sustained rise of [Ca(2+)](i) in a concentration-dependent manner (EC(50)=2.32 mM). DAS also induced a [Ca(2+)](i) elevation when extracellular Ca(2+) was removed, but the magnitude was reduced by 45%. Depletion of intracellular Ca(2+) stores with CCCP, a mitochondrial uncoupler, didn't affect DAS's effect. In Ca(2+)-free medium, the DAS-induced [Ca(2+)](i) rise was abolished by depleting stored Ca(2+) with thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor). DAS-caused [Ca(2+)](i) rise in Ca(2+)-containing medium was not affected by modulation of protein kinase C activity. The DAS-induced Ca(2+) influx was blocked by nicardipine. U73122, an inhibitor of phospholipase C, abolished ATP (but not DAS)-induced [Ca(2+)](i) rise. Additionally, pretreatment with DAS for 24 h decreased cell viability in a concentration-dependent manner. Furthermore, DAS-induced cell death involved apoptotic events. These findings suggest that diallyl sulfide induced a significant rise in [Ca(2+)](i) in MDCK renal tubular cells by stimulating both extracellular Ca(2+) influx and thapsigargin-sensitive intracellular Ca(2+) release via as yet unidentified mechanisms.
LanguageENG
Pub Type(s)JOURNAL ARTICLE
PubMed ID19555733
  
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