Document Detail


Treatment with docosahexaenoic acid, but not eicosapentaenoic acid, delays Ca2+-induced mitochondria permeability transition in normal and hypertrophied myocardium.
MedLine Citation:
PMID:  20624993     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intake of fish oil containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) prevents heart failure; however, the mechanisms are unclear. Mitochondrial permeability transition pore (MPTP) opening contributes to myocardial pathology in cardiac hypertrophy and heart failure, and treatment with DHA + EPA delays MPTP opening. Here, we assessed: 1) whether supplementation with both DHA and EPA is needed for optimal prevention of MPTP opening, and 2) whether this benefit occurs in hypertrophied myocardium. Rats with either normal myocardium or cardiac hypertrophy induced by 8 weeks of abdominal aortic banding were fed one of four diets: control diet without DHA or EPA or diets enriched with either DHA, EPA, or DHA + EPA (1:1 ratio) at 2.5% of energy intake for 17 weeks. Aortic banding caused a 27% increase in left ventricular mass and 25% depletion in DHA in mitochondrial phospholipids in rats fed the control diet. DHA supplementation raised DHA in phospholipids ∼2-fold in both normal and hypertrophied hearts and increased EPA. DHA + EPA supplementation also increased DHA, but to a lesser extent than DHA alone. EPA supplementation increased EPA, but did not affect DHA compared with the control diet. Ca(2+)-induced MPTP opening was delayed by DHA and DHA + EPA supplementation in both normal and hypertrophied hearts, but EPA had no effect on MPTP opening. These results show that supplementation with DHA alone effectively increases both DHA and EPA in cardiac mitochondrial phospholipids and delays MPTP and suggest that treatment with DHA + EPA offers no advantage over DHA alone.
Authors:
Ramzi J Khairallah; Karen M O'Shea; Bethany H Brown; Nishanth Khanna; Christine Des Rosiers; William C Stanley
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-07-12
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  335     ISSN:  1521-0103     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-21     Completed Date:  2010-10-21     Revised Date:  2012-05-07    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  155-62     Citation Subset:  IM    
Affiliation:
Division of Cardiology and Department of Medicine, University of Maryland, Baltimore, MD 21201, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arachidonic Acid / metabolism
Calcium / pharmacology*
Cardiomegaly / metabolism*,  ultrasonography
Diet
Dietary Supplements
Docosahexaenoic Acids / metabolism,  pharmacology*
Eicosapentaenoic Acid / metabolism,  pharmacology*
Electrocardiography
Fatty Acids / metabolism
Male
Mitochondria, Heart / drug effects,  metabolism*
Myocardium / metabolism
Oxygen Consumption / drug effects
Permeability / drug effects
Phospholipids / metabolism
RNA, Messenger / biosynthesis,  isolation & purification
Rats
Rats, Wistar
Triglycerides / metabolism
Grant Support
ID/Acronym/Agency:
HL074237/HL/NHLBI NIH HHS; HL091307/HL/NHLBI NIH HHS; HL101434/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids; 0/Phospholipids; 0/RNA, Messenger; 0/Triglycerides; 1553-41-9/Eicosapentaenoic Acid; 25167-62-8/Docosahexaenoic Acids; 506-32-1/Arachidonic Acid; 7440-70-2/Calcium
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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