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Reactive species of oxygen (ROS), responsible for oxidative stress, accumulate in various tissues damaged by burns, decubitus ulcers, and vascular lesions. Antioxidants play an important and well-documented role in healing of chronic and acute wounds. Rigenase®, a specific extract of Triticum vulgare manufactured by Farmaceutici Damor, is employed in products used for the regeneration of tissue injuries. In this work, we show that Rigenase® exhibits a scavenging effect toward free radicals, thus pointing to its relevant antioxidant activity.

Nitric oxide (NO) is critical for the normal physiological regulation of the nervous system and other tissues. L-Arginine, but not D-arginine, is the natural substrate for nitric oxide synthase (NOS), for it is enzymatically converted to NO and L-citrulline. However, recent evidence suggests that D-arginine can also produce NO and NO-derivatives via a different pathway. The aim of the present paper was to raise NO levels in the cells by increasing the cell permeation of its precursors. To this aim, two galactosyl prodrugs, L-arginine-D-galactos-6'-yl ester (L-ArgGal) and D-arginine-D-galactos-6'-yl ester (D-ArgGal) were synthesized. Remarkably, using the HPLC-ESI/MS technique, we found that L-ArgGal and D-ArgGal prodrugs both increased the concentration levels of L- and D-arginine and their derivatives in pituitary GH3 cells. Furthermore, we found that D-ArgGal (1) penetrated cell membranes more rapidly than its precursor D-arginine, (2) released arginine more slowly and in greater amounts than L-ArgGal, and (3) produced much higher levels of DAF-2 monitored NO and nitrite than did L-ArgGal under the same experimental conditions. In conclusion, these results indicate that an increase in the cell permeation of L- and D-arginine by L-ArgGal and D-ArgGal can lead to an increase in NO levels.