Polyphenols, mechanisms inhibition, oxidative stress

NADPH oxidase activity in circulating neutrophils (unpublished observations). NADPH oxidase-dependent superoxide production appears to be abnormally high in mononuclear cells from these patients (Formno et al. 2005). The absence of a commercial pharmacological treatment to reduce or inhibit systemic NADPH oxidase enzyme complex highlights the importance of our results, which demonstrate for the first time that the oxidative stress produced by systemic NADPH oxidase may be counteracted by supplementation with polyphenols. Our in vitro studies suggest that the mechanism involved in this effect is the reduction of p22phox, p47phox, and NOX expression (unpublished observations). 

Recently, in an approach to explain the diverse actions of polyphenols, Howitz et al. suggested that the antiproliferative and oncosuppressive properties of resveratrol might be due to a mechanism that mimics caloric restriction and lifespan extension, and involves the sirtuin (SIRT) family of nicotinamide adenine dinucleotide (NAD) -dependent acety-lases (Howitz et al. 2003). More specifically, resveratrol was found to directly interact with SIRTl deacetylase, resulting in decreased acetylation of p53, increased DNA stability, and finally cell survival. Redox formation was implicated in the inhibition of histone deacetylase (HDAC) activity, leading to a chronic inflammatory-like response (Rahman et al. 2004). In this respect, resveratrol is a promising agent in the reversal of oxidative stress and rescue of mutant phenotypes. 

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