Phenolic compounds (PC) have been proposed as natural antioxidant agents that protect cells against oxidative stress-related diseases. Nonetheless, their low bioavailability forecasts controversy about mechanisms on their in vivo scavenging activity against reactive oxygen species (ROS). It has been proposed that PC reduce directly ROS concentration. An alternative or complementary action of PC could be the activation of the cell's antioxidant pathway, involving the regulation of gene expression, like that initiated by the Nrf2 transcription factor. To date there is not enough experimental data to support or discard this possibility. In the present study, we evaluated the use of several PC to prevent peroxidation of macromolecules and to elicit the activation of the Nrf2 transcription factor in H2O2-stresed IEC-6 enterocytic cell line. Synchrotron microspectroscopy demonstrated that PC compounds protected proteins, lipids and nucleic acids against oxidation induced by H2O2. Immunofluorescence results showed that treatment with quercetin (Qc), catechin (Cat) and capsaicin (Cap) induced the translocation of Nrf2 into the nucleus, at the same level as did H2O2 treatment, thus mimicking the action of the endogenous cell response to peroxidation. Even though the detailed mechanism still needs to be elucidated, we demonstrated the activation of Nrf2 by PCs in response to oxidative stress.
Keywords: Flavonoids; IR spectroscopy; Immunofluorescence microscopy; Nrf2; Reactive oxygen species (ROS).
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