Document Detail

Mitochondrial-driven ubiquinone enhances extracellular calcium-dependent nitric oxide production and reduces glycochenodeoxycholic acid-induced cell death in hepatocytes.
MedLine Citation:
PMID:  20020783     Owner:  NLM     Status:  MEDLINE    
Ca(2+) mobilization, nitric oxide (NO), and oxidative stress have been involved in cell death induced by hydrophobic bile acid in hepatocytes. The aim of the study was the elucidation of the effect of the antioxidant mitochondrial-driven ubiquinone (Mito Q) on the intracellular Ca(2+) concentration, NO production, and cell death in glycochenodeoxycholic acid (GCDCA)-treated HepG2 cells. The role of the regulation of the intracellular Ca(2+) concentration by Ca(2+) chelators (EGTA or BAPTA-AM), agonist of Ca(2+) entrance (A23187) or NO (L-NAME or NO donor), was assessed during Mito Q cytoprotection in GCDCA-treated HepG2 cells. Cell death, NO synthase (NOS)-1, -2, and -3 expression, Ca(2+) mobilization, and NO production were evaluated. GCDCA reduced the intracellular Ca(2+) concentration and NOS-3 expression and enhanced cell death in HepG2. NO donor prevented and L-NAME enhanced GCDCA-induced cell death. The reduction of Ca(2+) entry by EGTA, but not its release from intracellular stores by BAPTA-AM, reduced the expression of NOS-3 and enhanced cell death in control and GCDCA-treated cells. Mito Q prevented the reduction of intracellular Ca(2+) concentration, NOS-3 expression, NO production, and cell death in GCDCA-treated HepG2 cells. The conclusion is that the recovery of Ca(2+)-dependent NOS-3 expression by Mito Q may be considered an additional cytoprotective property of an antioxidant.
Sandra Gonz?lez-Rubio; Ana B Hidalgo; Gustavo Ferr?n; Rosario I Bello; Raul Gonz?lez; Manuel D Gahete; Isidora Ranchal; Blanca A Rodr?guez; Pilar Barrera; Patricia Aguilar-Melero; Clara I Linares; Justo P Casta?o; Victor M Victor; Manuel De la Mata; Jordi Muntan?
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Chemical research in toxicology     Volume:  22     ISSN:  1520-5010     ISO Abbreviation:  Chem. Res. Toxicol.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-12-21     Completed Date:  2010-03-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8807448     Medline TA:  Chem Res Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1984-91     Citation Subset:  IM    
Liver Research Unit, Reina Sofia University Hospital, Cordoba, Spain.
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MeSH Terms
Apoptosis / drug effects*
Calcimycin / pharmacology
Calcium / metabolism*
Caspase 3 / metabolism
Glycochenodeoxycholic Acid / chemistry*,  toxicity
Hep G2 Cells
Hepatocytes / metabolism*
Mitochondria / metabolism*
Nitric Oxide / metabolism*
Nitric Oxide Synthase Type III / genetics,  metabolism
Ubiquinone / metabolism*
Reg. No./Substance:
10102-43-9/Nitric Oxide; 1339-63-5/Ubiquinone; 52665-69-7/Calcimycin; 640-79-9/Glycochenodeoxycholic Acid; 7440-70-2/Calcium; EC Oxide Synthase Type III; EC 3.4.22.-/Caspase 3

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