Chemisorption of water onto anhydrous nanophase manganese oxide surfaces promotes rapidly reversible redox phase changes as confirmed by calorimetry, X-ray diffraction, and titration for manganese average oxidation state. Surface reduction of bixbyite (Mn2O3) to hausmannite (Mn3O4) occurs in nanoparticles under conditions where no such reactions are seen or expected on grounds of bulk thermodynamics in coarse-grained materials. Additionally, transformation does not occur on nanosurfaces passivated by at least 2% coverage of what is likely an amorphous manganese oxide layer. The transformation is due to thermodynamic control arising from differences in surface energies of the two phases (Mn2O3 and Mn3O4) under wet and dry conditions. Such reversible and rapid transformation near room temperature may affect the behavior of manganese oxides in technological applications and in geologic and environmental settings.

Manganese oxides with layer and tunnel structures occur widely in nature and inspire technological applications. Having variable compositions, these structures often are found as small particles (nanophases). This study explores, using experimental thermochemistry, the role of composition, oxidation state, structure, and surface energy in the their thermodynamic stability. The measured surface energies of cryptomelane, sodium birnessite, potassium birnessite and calcium birnessite are all significantly lower than those of binary manganese oxides (Mn₃O₄, Mn₂O₃, and MnO₂), consistent with added stabilization of the layer and tunnel structures at the nanoscale. Surface energies generally decrease with decreasing average manganese oxidation state. A stabilizing enthalpy contribution arises from increasing counter-cation content. The formation of cryptomelane from birnessite in contact with aqueous solution is favored by the removal of ions from the layered phase. At large surface area, surface-energy differences make cryptomelane formation thermodynamically less favorable than birnessite formation. In contrast, at small to moderate surface areas, bulk thermodynamics and the energetics of the aqueous phase drive cryptomelane formation from birnessite, perhaps aided by oxidation-state differences. Transformation among birnessite phases of increasing surface area favors compositions with lower surface energy. These quantitative thermodynamic findings explain and support qualitative observations of phase-transformation patterns gathered from natural and synthetic manganese oxides.

Silica nanoparticles with iron on their surface cause the production of oxidants and stimulate an inflammatory response in macrophages. Nuclear factor erythroid-derived 2 - like factor 2 (Nrf2) signaling and its regulated antioxidant genes play critical roles in maintaining redox homeostasis. In this study we investigated the regulation of four representative Nrf2-regulated antioxidant genes; i.e., glutamate cysteine ligase (GCL) catalytic subunit (GCLC), GCL modifier subunit (GCLM), heme oxygenase 1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO-1), by iron-coated silica nanoparticles (SiO₂-Fe) in human THP-1 macrophages. We found that the expression of these four antioxidant genes was modified by SiO₂-Fe in a time-dependent manner. At 6h, their expression was unchanged except for GCLC, which was reduced compared with controls. At 18h, the expression of these antioxidant genes was significantly increased compared with controls. In contrast, the Nrf2 activator sulforaphane induced all antioxidant genes at as early as 3h. The nuclear translocation of Nrf2 occurred later than that for NF-κB p65 protein and the induction of proinflammatory cytokines (TNFα and IL-1β). NF-κB inhibitor SN50 prevented the reduction of GCLC at 6h and abolished the induction of antioxidant genes at 18h by SiO₂-Fe, but did not affect the basal and sulforaphane-induced expression of antioxidant genes, suggesting that NF-κB signaling plays a key role in the induction of Nrf2-mediated genes in response to SiO₂-Fe. Consistently, SN50 inhibited the nuclear translocation of Nrf2 caused by SiO₂-Fe. In addition, Nrf2 silencing decreased the basal and SiO₂-induced expression of the four reprehensive antioxidant genes. Taken together, these data indicated that SiO₂-Fe induced a delayed response of Nrf2-regulated antioxidant genes, likely through NF-κB-Nrf2 interactions.

Silica nanoparticles with iron on their surface cause the production of oxidants and stimulate an inflammatory response in macrophages. Nuclear factor erythroid-derived 2 - like factor 2 (Nrf2) signaling and its regulated antioxidant genes play critical roles in maintaining redox homeostasis. In this study we investigated the regulation of four representative Nrf2-regulated antioxidant genes; i.e., glutamate cysteine ligase (GCL) catalytic subunit (GCLC), GCL modifier subunit (GCLM), heme oxygenase 1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO-1), by iron-coated silica nanoparticles (SiO₂-Fe) in human THP-1 macrophages. We found that the expression of these four antioxidant genes was modified by SiO₂-Fe in a time-dependent manner. At 6h, their expression was unchanged except for GCLC, which was reduced compared with controls. At 18h, the expression of these antioxidant genes was significantly increased compared with controls. In contrast, the Nrf2 activator sulforaphane induced all antioxidant genes at as early as 3h. The nuclear translocation of Nrf2 occurred later than that for NF-κB p65 protein and the induction of proinflammatory cytokines (TNFα and IL-1β). NF-κB inhibitor SN50 prevented the reduction of GCLC at 6h and abolished the induction of antioxidant genes at 18h by SiO₂-Fe, but did not affect the basal and sulforaphane-induced expression of antioxidant genes, suggesting that NF-κB signaling plays a key role in the induction of Nrf2-mediated genes in response to SiO₂-Fe. Consistently, SN50 inhibited the nuclear translocation of Nrf2 caused by SiO₂-Fe. In addition, Nrf2 silencing decreased the basal and SiO₂-induced expression of the four reprehensive antioxidant genes. Taken together, these data indicated that SiO₂-Fe induced a delayed response of Nrf2-regulated antioxidant genes, likely through NF-κB-Nrf2 interactions.