Supforaphane as a new cardioprotecitive agent against oxidative damage.

The increasing recognition of the role of oxidative stress in the pathophysiology of cardiovascular diseases has led to extensive investigation on the protection against oxidative cardiac injury by exogenous antioxidants Several naturally occurring compounds are known to present detoxicating properties in different mammalian cells, mostly by their ability to induce Phase II enzymes, but data on the ability of functional components of food to increase endogenous antioxidant defences are lacking. As an important consequence of Phase II enzyme induction is the enhancement of cellular antioxidant capacity, the up-regulation of endogenous antioxidant systems may represent a promising strategy for protecting cells against oxidative damage. Using cultured rat cardiomyocytes we have characterized the time-dependent induction of cellular antioxidants and Phase II enzymes by sulforafane (SF), a potent natural chemopreventive compound present in substantial quantities in the human diet (primarily originating from the ingestion of Cruciferous vegetables). Incubation of cardiomyocytes with SF resulted in a marked increase of glutathio reductase, glutathione-S-tranferase and quinone reductase 1 activity and expression and of intracellular GSH (the most prominent intracellular thiol in the heart) levels. SF pretreatment caused a decreased intracellular accumulation of ROS and an increased cell viability in comparison to cells exposed to oxidants. Our results demonstrate that SF influences the intracellular redox environment up-regulating antioxidant cellular defences, thus acting as an indirect antioxidant leading to cardioprotection against oxidative damage Supported by MIUR and Fondazione del Monte di BO e RA (Italy