2Chapter 0 Oxidative Metabolites of Lycopene and Their Biological Functions
Considerable interest and research efforts have been expended in an effort to uncover the potential roles of carotenoids in human health and disease. While early studies focused on provitamin A carotenoids, more recent research efforts have focused on the potential roles of the non-provitamin A carotenoids (e.g., lycopene) in the health and the disease. Lycopene has been implicated as having a potential bene cial impact in a number of chronic diseases including cancer. Although evidence from epidemiological and animal studies supports a potential chemopreventive role of lycopene (Boileau et al. 2003, Canene-Adams et al. 2007, Giovannucci 1999b, Giovannucci and Clinton 1998, Siler et al. 2004), the biochemical mechanisms behind such bene cial effects have, as of yet, not been wellde ned. Several reports have demonstrated the potential bene cial effects of lycopene especially in respect to antioxidant function, enhanced cellular gap junction communication, the induction of phase II enzymes through the activation of the antioxidant response element (ARE) transcription system, the suppression of insulin-like growth factor (IGF)-1 stimulated cell proliferation by induced
insulin-like growth factor binding protein (IGFBP), and the inhibition of cell proliferation and the induction of apoptosis. With the cloning and the characterization of two distinct carotenoid cleaving enzymes, recent research has focused on the metabolic fate of lycopene and the subsequent metabolites created. Several reports, including our own, suggest that the biological activities of lycopene may be mediated, in part, by lycopene metabolites. Lycopene metabolites, and carotenoid metabolites in general, can possess either more or less activity than the parent compound or can have an entirely independent function. The chemical and biological metabolisms of lycopene and the potential actions of lycopene and its metabolites on chemoprevention will be highlighted in this chapter.