Abstract

The research conducted so far has shown that endogenous antioxidants, despite being regarded as the first line of antioxidant defense, may not be sufficient to maintain redox homeostasis in cells exposed to oxidative stress. The results obtained in the doctoral dissertation show that endogenous redox-active compounds were moderate or weak scavengers of ABTS and DPPH radicals, while in cellular setting, their impact on the reducing capacity of HT29 cells was diversified. The results showed no significant correlation between the cellular antioxidant activity and electrochemical properties of tested compounds. Better compliance with biological activity was found for the kinetic parameter describing the velocity of neutralization of ABTS and DPPH radicals. Most of the tested redox-active compounds did not have significant impact on growth of HT29 cells. The inhibition of growth was observed solely in the case of high concentrations. Endogenous redox-active compounds did not protect DNA from fragmentation induced by oxidants in HT29 cells. The obtained results showed that endogenous redox-active compounds display weaker antioxidant activity compared to exogenous antioxidants. This research provided the systematic evidence that the maintenance of redox homeostasis, should the oxidative stress challenge occur, requires the support of exogenous dietary antioxidants.

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