Polyphenol tannic acid inhibits hydroxyl radical formation from Fenton reaction by complexing ferrous ions.

Abstract Tannic acid (TA), a plant polyphenol, has been described as having antimutagenic, anticarcinogenic and antioxidant activities. Since it is a potent chelator of iron ions, we decided to examine if the antioxidant activity of TA is related to its ability to chelate iron ions. The degradation of 2-deoxyribose induced by 6 μM Fe(II) plus 100 μM H 2 O 2 was inhibited by TA, with an I 50 value of 13 μM. Tannic acid was over three orders of magnitude more efficient in protecting against 2-deoxyribose degradation than classical ⋅ OH scavengers. The antioxidant potency of TA was inversely proportional to Fe(II) concentration, demonstrating a competition between H 2 O 2 and AT for reaction with Fe(II). On the other hand, the efficiency of TA was nearly unchanged with increasing concentrations of the ⋅ OH detector molecule, 2-deoxyribose. These results indicate that the antioxidant activity of TA is mainly due to iron chelation rather than ⋅ OH scavenging. TA also inhibited 2-deoxyribose degradation mediated by Fe(III)-EDTA (iron=50 μM) plus ascorbate. The protective action of TA was significantly higher with 50 μM EDTA than with 500 μM EDTA, suggesting that TA removes Fe(III) from EDTA and forms a complex with iron that cannot induce ⋅ OH formation. We also provided evidence that TA forms a stable complex with Fe(II), since excess ferrozine (14 mM) recovered 95–96% of the Fe(II) from 10 μM TA even after a 30-min exposure to 100–500 μM H 2 O 2 . Addition of Fe(III) to samples containing TA caused the formation of Fe(II) n –TA, complexes, as determined by ferrozine assays, indicating that TA is also capable of reducing Fe(III) ions. We propose that when Fe(II) is complexed to TA, it is unable to participate in Fenton reactions and mediate ⋅ OH formation. The antimutagenic and anticarcinogenic activity of TA, described elsewhere, may be explained (at least in part) by its capacity to prevent Fenton reactions.