The effect of the dietary constituent conjugated linoleic acid and homocysteine on vascular endothelial cell function
Coen, Paul Martin (2004) The effect of the dietary constituent conjugated linoleic acid and homocysteine on vascular endothelial cell function. Master of Science thesis, Dublin City University.
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The interaction between circulating dietary constituents and the vascular endothelial monolayer is vital to the proper maintenance o f vascular homeostatic mechanisms, such as vasoregulation. Endothelial dysfunction with subsequent loss of vasoregulatory function are implicated in the early stages of atherosclerosis. Conjugated linoleic acid (CLA) and homocysteine are dietary constituents that have been implicated in the aetiology of atherosclerosis.
CLA is the collective term used for positional and geometrical isomers deriving from the essential fatty acid, linoleic acid. Previous studies have indicated an atheroprotective effect of CLA , manifested in slowing atherosclerotic plaque formation. CLA may be eliciting these effects via two potential mechanisms. Firstly, CLA may be auto oxidised to several furan derivatives that possess a redox buffering capacity, and may modulate endothelium exposure to oxidative stress. Secondly, the influence of CLA on the production of Cyclooxygenase (Cox) derived eicosanoids, such as prostacyclin, has also been suggested as a possible mechanism of action. Homocysteine is a sulphur-containing amino acid formed during the metabolism of methionine. Numerous studies have shown that hyperhomocysteinemia is an independent risk factor for atherosclerosis and atherothrombos. Prolonged exposure and high homocysteine concentrations result in impaired nitric oxide production and subsequent vascular endothelial dysfunction.
The objective of this study was to investigate whether both C L A and/or homocysteine modulate the expression and/or activity o f two distinct vascular endothelial cell (EC) components; Nitric oxide synthase (eNOS) and Cox. Both eNOS and Cox, responsible for production o f nitric oxide and prostacyclin respectively, have been strongly implicated in the endothelial maintenance of vascular hemodynamic mechanisms.
The results from this study suggest that CLA downregulates endothelial release of prostacyclin (PGI2) and probably many other prostanoids (PGE2 and PGD2) CLA isomer mix does appear to putatively modulate prostanoid production and agoniststimulated nitric oxide release from BAEC.
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