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Research: DABKOWSKI and COLLEAGUES,
Listed in Issue 244
Abstract
DABKOWSKI and COLLEAGUES, (1)Division of Cardiology, Department of Medicine, University of Maryland, Baltimore, MD, USA assessed in rats the effects of DHA supplementation on cardiac mitochondria and the development of heart failure caused by aortic pressure overload.
Background
Supplementation with the n3 polyunsaturated fatty acid docosahexaenoic acid (DHA) is beneficial in heart failure patients, however the mechanisms are unclear. DHA is incorporated into membrane phospholipids, which may prevent mitochondrial dysfunction. Thus the authors assessed the effects of DHA supplementation on cardiac mitochondria and the development of heart failure caused by aortic pressure overload.
Methodology
Pathological cardiac hypertrophy was generated in rats by thoracic aortic constriction. Animals were fed either a standard diet or were supplemented with DHA (2.3 % of energy intake).
Results
After 14 weeks, heart failure was evident by left ventricular hypertrophy and chamber enlargement compared to shams. Left ventricle fractional shortening was unaffected by DHA treatment in sham animals (44.1 ± 1.6 % vs. 43.5 ± 2.2 % for standard diet and DHA, respectively), and decreased with heart failure in both treatment groups, but to a lesser extent in DHA treated animals (34.9 ± 1.7 %) than with the standard diet (29.7 ± 1.5 %, P < 0.03). DHA supplementation increased DHA content in mitochondrial phospholipids and decreased membrane viscosity. Myocardial mitochondrial oxidative capacity was decreased by heart failure and unaffected by DHA. DHA treatment enhanced Ca(2+) uptake by subsarcolemmal mitochondria in both sham and heart failure groups. Further, DHA lessened Ca(2+)-induced mitochondria swelling, an index of permeability transition, in heart failure animals. Heart failure increased hydrogen peroxide-induced mitochondrial permeability transition compared to sham, which was partially attenuated in interfibrillar mitochondria by treatment with DHA.
Conclusion
DHA decreased mitochondrial membrane viscosity and accelerated Ca(2+) uptake, and attenuated susceptibility to mitochondrial permeability transition and development of left ventricular dysfunction.
References
Dabkowski ER(1), O'Connell KA, Xu W, Ribeiro RF Jr, Hecker PA, Shekar KC, Daneault C, Des Rosiers C, Stanley WC. Docosahexaenoic acid supplementation alters key properties of cardiac mitochondria and modestly attenuates development of left ventricular dysfunction in pressure overload-induced heart failure. Cardiovasc Drugs Ther. 27(6):499-510. doi: 10.1007/s10557-013-6487-4. Dec 2013.