Numerous epidemiologic studies showed an inverse correlation
between dietary flavonoid consumption and cardiovascular risk, but the exact
mechanisms are still largely unknown. Flavonoids exhibit hormetic properties,
where low concentrations activate adaptive cellular stress response pathways
and thus lead towards cytoprotection, whereas high concentrations are
cytotoxic. However, the limited bioavailability of dietary flavonoids doubts the
relevance of effective flavonoid intracellular concentrations to induce bioactivity
in endothelial cells. Therefore, translocation of flavonoids through the cell plasma
membrane must occur via specific transporter proteins. Hereby, we describe the
involvement of the membrane transporter bilitranslocase (TC #2.A.65.1.1) as
the key underlying molecular mechanism for membrane transport, which might
help resolve the enigma of flavonoids bioactivity.
