(−)-Epigallocatechin-(3)-gallate prevents oxidative damage in both the aqueous and lipid compartments of human plasma

Abstract

When human plasma was exposed to the hydrophilic radical initiator, AAPH, (−)-epigallocatechin-(3)-gallate (EGCG) dose-dependently inhibited the aqueous compartment oxidation ( IC 50=0.72 μM ) (monitored by DCFH oxidation) and spared the lipophilic antioxidants, α-tocopherol, and carotenoids, but not ascorbic acid. When radicals were selectively induced in the lipid compartment by the lipophilic radical initiator, MeO-AMVN, EGCG spared α-tocopherol, but not carotenoids and inhibited the lipid compartment oxidation (monitored by BODIPY 581/591) with a potency lower than that found in the aqueous compartment ( IC 50=4.37 μM ). Our results indicate that EGCG, mainly localized in the aqueous compartment, effectively quenches aqueous radical species, thus limiting their diffusion into the lipid compartment and preventing lipid-soluble antioxidant depletion. Further, ESR experiments confirmed that EGCG recycled α-tocopherol through a H-transfer mechanism at the aqueous/lipid interface affording an additional protective mechanism to the lipid compartment of plasma.