PMID- 22653687
OWN - NLM
STAT- MEDLINE
DCOM- 20130528
LR  - 20161125
IS  - 1477-0903 (Electronic)
IS  - 0960-3271 (Linking)
VI  - 31
IP  - 12
DP  - 2012 Dec
TI  - Effect of phenethyl isothiocyanate on Ca2+ movement and viability in MDCK canine 
      renal tubular cells.
PG  - 1251-61
LID - 10.1177/0960327112446841 [doi]
AB  - The effect of the natural compound phenethyl isothiocyanate (PEITC) on cytosolic 
      Ca(2+) concentrations ([Ca(2+)](i)) and viability in MDCK renal cells is unknown. 
      This study explored whether PEITC changed [Ca(2+)](i) in MDCK cells using the 
      Ca(2+)-sensitive fluorescent dye fura-2. PEITC at 200-700 muM increased 
      [Ca(2+)](i) in a concentration-dependent manner. The signal was reduced by 
      removing extracellular Ca(2+). PEITC-induced Ca(2+) influx was inhibited by 
      nifedipine, econazole, SK&F 96365 and protein kinase C modulators. In Ca(2+)-free 
      medium, treatment with the endoplasmic reticulum Ca(2+) pump inhibitor 
      thapsigargin (TG) or 2,5-di-tert-butylhydroquinone (BHQ) inhibited PEITC-induced 
      rise in [Ca(2+)](i). Incubation with PEITC also inhibited TG or BHQ-induced rise 
      in [Ca(2+)](i). Inhibition of phospholipase C with U73122 abolished PEITC-induced 
      rise in [Ca(2+)](i). At 15-75 muM, PEITC decreased viability. The cytotoxic effect 
      of PEITC was enhanced by chelating cytosolic Ca(2+) with 
      1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester. 
      Annexin V-FITC data suggest that 20 and 50 muM PEITC induced apoptosis. At 10 and 
      15 muM, PEITC did not increase reactive oxygen species (ROS) production. Together, 
      in renal tubular cells, PEITC-induced rise in [Ca(2+)](i) by inducing 
      phospholipase C-dependent Ca(2+) release from endoplasmic reticulum and Ca(2+) 
      entry via store-operated Ca(2+) channels. PEITC induced apoptosis in a 
      concentration-dependent, ROS/Ca(2+)-independent manner.
FAU - Chen, I S
AU  - Chen IS
AD  - Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
FAU - Mok, K T
AU  - Mok KT
FAU - Chou, C T
AU  - Chou CT
FAU - Liu, S I
AU  - Liu SI
FAU - Kuo, C C
AU  - Kuo CC
FAU - Hsu, S S
AU  - Hsu SS
FAU - Chang, H T
AU  - Chang HT
FAU - Tsai, J Y
AU  - Tsai JY
FAU - Liao, W C
AU  - Liao WC
FAU - Jan, C R
AU  - Jan CR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120531
PL  - England
TA  - Hum Exp Toxicol
JT  - Human & experimental toxicology
JID - 9004560
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (Isothiocyanates)
RN  - 139890-68-9 (1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid 
      acetoxymethyl ester)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 67526-95-8 (Thapsigargin)
RN  - 6U7TFK75KV (phenethyl isothiocyanate)
RN  - 6Z1Y2V4A7M (Econazole)
RN  - I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole)
RN  - I9ZF7L6G2L (Nifedipine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Calcium/*metabolism
MH  - Calcium Signaling/*drug effects/physiology
MH  - Cell Survival/drug effects
MH  - Cytosol/drug effects/metabolism
MH  - Dogs
MH  - Econazole/pharmacology
MH  - Egtazic Acid/analogs & derivatives/pharmacology
MH  - Enzyme Inhibitors/*toxicity
MH  - Imidazoles/pharmacology
MH  - Isothiocyanates/*toxicity
MH  - Kidney Tubules/*drug effects/metabolism/pathology
MH  - Madin Darby Canine Kidney Cells
MH  - Nifedipine/pharmacology
MH  - Thapsigargin/pharmacology
EDAT- 2012/06/02 06:00
MHDA- 2013/05/29 06:00
CRDT- 2012/06/02 06:00
PHST- 2012/06/02 06:00 [entrez]
PHST- 2012/06/02 06:00 [pubmed]
PHST- 2013/05/29 06:00 [medline]
AID - 0960327112446841 [pii]
AID - 10.1177/0960327112446841 [doi]
PST - ppublish
SO  - Hum Exp Toxicol. 2012 Dec;31(12):1251-61. doi: 10.1177/0960327112446841. Epub 
      2012 May 31.