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. 2013 Oct;57(10):1814-24.
doi: 10.1002/mnfr.201300133. Epub 2013 Jun 10.

Methionine-induced hyperhomocysteinemia impairs the antioxidant ability of high-density lipoproteins without reducing in vivo macrophage-specific reverse cholesterol transport

Josep Julve  1 , Joan C Escolà-Gil, Elisabeth Rodríguez-Millán, Jesús M Martín-Campos, Matti Jauhiainen, Helena Quesada, Ivy M Rentería-Obregón, Jesús Osada, José L Sánchez-Quesada, Francisco Blanco-Vaca
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Methionine-induced hyperhomocysteinemia impairs the antioxidant ability of high-density lipoproteins without reducing in vivo macrophage-specific reverse cholesterol transport

Josep Julve et al. Mol Nutr Food Res. 2013 Oct.

Abstract

Scope: High plasma homocysteine concentrations have been associated with increased risk of cardiovascular disease both in humans and experimental animal models, whereas plasma HDL-cholesterol concentration is inversely correlated with such disorders. This work aimed to study the impact of methionine-induced hyperhomocysteinemia (HHcy) on two major antiatherogenic functions of HDL, namely their capacity to prevent LDL oxidation and induce in vivo macrophage-specific reverse cholesterol transport.

Methods and results: Methionine-induced HHcy in mice resulted in an approximately 20% decreased concentration of HDL-cholesterol and HDL main protein component, apolipoprotein A-I. The HDL potential to resist oxidation as well as to prevent LDL oxidative modification was impaired in hyperhomocysteinemic mice. Activities of paraoxonase-1 and platelet activation factor acetylhydrolase, two of the main HDL-associated enzymes with antioxidant activity, were reduced. The ability of HDL to efflux cholesterol from macrophages was decreased in hyperhomocysteinemic mice; however, the in vivo macrophage-specific reverse cholesterol transport measured as the output of labeled cholesterol into feces did not significantly differ between groups.

Conclusion: Our data indicate that the HDL from methionine-induced hyperhomocysteinemic mice was more prone to oxidation and displayed lower capacity to protect LDL against oxidative modification than that of control mice, highlighting a mechanism by which a diet-induced HHcy may facilitate progression of atherosclerosis.

Keywords: HDL; Homocysteine; Hyperhomocysteinemia; Methionine; Oxidation; Reverse cholesterol transport.

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