Resveratrol (3,4',5-trihydroxystilbene) is a natural phytoalexin synthesized in response to injury or fungal attack, found in the grape skin and wine, specially red wine. A large number of studies have demonstrated that
resveratrol regulates many
biological activities, namely protection against
atherosclerosis by a set of pharmacological properties, including the
antioxidant activity. In this study, we explored the capacity of
resveratrol in protecting
low density lipoproteins (
LDL) against either
ferrylmyoglobin- or
peroxynitrite-mediated oxidation and the underlying mechanisms of its
antioxidant potential.
Resveratrol efficiently decreases the accumulation of hydroperoxides in
LDL promoted by
ferrylmyoglobin, a potent
oxidant formed by the reaction of
metmyoglobin with
hydrogen peroxide, in a concentration-dependent manner, promptly reducing the oxoferryl complex to
metmyoglobin. Simultaneously,
resveratrol is consumed as detected by the rapid decrease in the characteristic peak at 310 nm, in a similar way to that observed upon its reaction with
peroxidase/H2O2, pointing to a mechanism of one-electron oxidation and subsequent
resveratrol dimer formation. On the other hand,
resveratrol inhibits
LDL apoprotein modifications induced by
peroxynitrite, another potent
oxidant formed by the reaction between
superoxide and
nitric oxide, as assessed by the decrease in
apo-B net charge alterations and in carbonyl groups formation mediated by that
oxidant.
Resveratrol also interacts with
peroxynitrite in a similar way to that observed with laccases, suggesting a mechanism of
resveratrol oxidation rather than a nitration one. These mechanisms are discussed. Considering that either
ferrylmyoglobin or
peroxynitrite are physiologically relevant
oxidants implicated in several pathologies, including
atherosclerosis, our results certainly contribute to the understanding of the
antioxidant action of
resveratrol and consequently provide a new approach for the cardiovascular benefits associated with moderate consumption of red wine.