Oyster ferritin can efficiently alleviate ROS-mediated inflammation attributed to its unique micro-environment around three-fold channels.

The conversion of toxic Fe2+ into non-toxic Fe3+ stored in the inner cavity of ferritin nanocage could effectively reduce the occurrence of the Fenton reaction and inhibit the formation of harmful reactive oxygen species (ROS). In this study, we reveal that oyster ferritin (GF1) can rely on its high catalytic activity (7.7 times that of rHuHF) and high binding ability of Fe2+ (9.1 times that of rHuHF) to reduce the precursors of Fenton reaction, thus inhibiting the occurrence of Fenton reaction and slowing down reactive oxygen species-mediated inflammation. The above significant advantage of GF1 can be attributed to the Asp at the position 120th, which could increase the negatively charged area of three-fold channels from 37.8% (rHuHF) to 67.8% and then enhance its oxidation rate and ability of GF1. The findings are of great value in advancing novel nanoparticle drug design based on crystalline structure. [Display omitted] • Asp120 of oyster ferritin had a contribution to the catalytic oxidation rate of Fe2+. • Oyster ferritin shows the catalytic activity of 7.7 times higher than that of rHuHF. • Oyster ferritin shows the binding ability of 9.1 times higher than that of rHuHF. • Oyster ferritin could significantly reduce the precursors of Fenton reaction. [ABSTRACT FROM AUTHOR]