“…This should be due to the strong electrophilicity of the (-peroxo)(-oxo)-diiron(III) species (species (A) in Scheme I) formed in the solution (Nishida, 2003(Nishida, , 2004(Nishida, , 2011(Nishida, , 2012a(Nishida, , 2012b, which turns to the di--oxo-diiron(III) species by oxidizing the methanol in the solution The further aggregation of the di--oxo-diiron(III) species may proceed to give the iron deposition (see (C) in Scheme I), because it has been pointed out that the iron deposition is the aggregation of di--oxo-diiron (III) species based on the structural properties of hydroxo(oxo)iron clusters (Nishida, 2012a(Nishida, , 2012c; this is exemplified by the recent our work (Abe, Sakiyama & Nishida, 2015a). As these polymeric iron(III) ions are not transferred to apo-transferrin (Nishida, Ito & Satoh, 2007;Nishida, 2012c), above discussion explains the marked iron accumulation in the brain as well as visceral tissue despite low serum iron levels, and under these conditions where excess hydrogen peroxide is present. It seems quite likely that highly toxic (-peroxo)diiron(III) species ((A) in Scheme I) generates in a facile manner, degrading the peripheral proteins or DNA, inducing severe oxidative damage, which are all consistent with those observed in the aceruroplasminemia patients (Yoshida, et al 2000), where in the patient of aceruroplasminemia, Fe 2+ ions are oxidized by apo-transferrin to Fe 3+ ions with the formation of hydrogen peroxide (Nishida, 2012c).…”