Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 16 No. 5 • May 2013


Arginine Update

Arginine Potently Prevents Formation of AGEs Protects Against Endothelial Dysfunction, Oxidative Stress, and Metabolic Syndrome

A new paper1 reports on highly protective effects of L-arginine (and also D-arginine) against endothelial dysfunction, increased AGE (advanced glycation endproduct) formation, and other features characteristic of type 2 diabetes by scavenging of methylglyoxal, a reactive dicarbonyl molecule produced during glucose, fatty acid, and amino acid metabolism that is a major precursor in the formation of AGEs.

The authors note that there is currently a lack of specific scavengers for methylglyoxal (MG), but that MG has been reported to have a high affinity for arginine. Hence, they tested the protective effects of arginine on the vascular smooth muscle cells and isolated aortic rings derived from rats and then incubated in high glucose (25mM) or methylglyoxal (MG) 100 mM) and tested for relaxation in response to acetylcholine.

Results showed that D-arginine and L-arginine prevented high glucose-induced elevation of MG levels in vascular smooth muscle cells and rat isolated aorta. MG and high glucose increased the expression and activity of the enzyme arginase (an enzyme in the urea cycle that catalyzes the formation of urea and ornithine) which competes with NOS (nitric oxide synthase) for L-arginine. Hence, increase in arginase can reduce the availability of arginine for conversion to nitric oxide by NOS, thus inducing endothelial dysfunction.

Another result of the study was the finding that D-arginine, L-arginine, and N-acetylcysteine prevented MG and high glucose-induced formation of the methylglyoxal-specific advanced glycation endproduct (AGE) N-carboxyethyl lysine (CEL). Coincubation of vascular smooth muscle cells with D-Arg (300 μM), L-Arg (300 μM) or NAC (N-acetylcysteine) (600 μM) attenuated the formation of CEL.

The authors note that, because L-Arg, but not D-Arg, is a precursor for NOS (nitric oxide synthase) and because D-Arg as well as L-Arg prevented MG- and high glucose-induced reduced relaxation, they conclude that “it strongly suggests that arginine, especially D-Arg, prevents MG- and high glucose-induced reduced relaxation by an eNOS-independent mechanism.” “The therapeutic potential of arginine against MG and high-glucose-induced pathology merits further investigation.”1

Reference

  1. Dhar et al. Arginine attenuates methylglyoxal- and high glucose-induced endothelial dysfunction and oxidative stress by an endothelial nitric-oxide synthase-independent mechanism. J Pharmacol Exp Ther. 342(1): 196-204 (2012).

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