The measurement of the total antioxidant capacity (TAC) of human plasma has been applied in the nutrition science in several ways. In particular, it has been used to evaluate the antioxidant contributions of dietary components and to study the bioavailability of dietary antioxidant nutrients.
Several methods have been recently proposed for the measurement of the TAC in human plasma, most of them based on the measurement of the ability of plasma to withstand the oxidative damage induced by aqueous radical initiator such as AAPH or transition metal ions. However, as the oxidation process is induced primarily by hydrophilic radicals and measures the aqueous plasma compartment oxidizability, these methods are unable to determine the antioxidant capacity of the lipid compartment. It is nut surprising that most of the methods used to measure the total antioxidant capacity of plasma such as TRAP (Total Radical Trapping Antioxidant Parameter), ORaC (Oxygen I~_dical Absorbance Capacity), and FR-P (Ferric Reducing Ability of Plasma) failed to show any direct correlation between fat-soluble antioxidant nutrient levels and antioxidant capacity in circulation following a diet enriched with carotenoids[I-3 ]. These results can be explained by considering that the plasma carotenoids, being deeply embedded in the lipoprotein core, are not available for reacting with the aqueous radical species or ferric complexes.
The selective measurement of lipid compartment oxidizability could be relevant not only to study the effect of a diet supplemented with fat-soluble antioxidants, but also to investigate the lipoprotein oxidation in whole plasma and the activity and mechanism of both fat- and water- soluble antioxidants. Therefore, we firstly focused our interest on de-lipid probe, but with a potency lower than that found in the aqueous compartment (ICS.=4.37 pM). The results indicate that EGCG at concentrations found in human plasma after acute or chronic green tea ingestion is mainly localized in the aqueous compartment, where it is effective in quenching aqueous radical species, thus limiting their diffusion into the lipid compartment and preventing lipid-soluble antioxidant depletion. EGCG is also able to interact with - tocopherol at the aqueous/lipid interface where recycling of -tocopherol occurs through an H-transfer mechanism, as confirmed by ESR experiments, affording an additional protective mechanism to the lipid compartment of plasma.
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