Abstract[ThB5O6(OH)6][BO(OH)2]·2.5H2O (Notre Dame Thorium Borate‐1, NDTB‐1) is an inorganic supertetrahedral cationic framework material that is derived from boric acid flux reactions. NDTB‐1 exhibits facile single crystal to single crystal anion exchange with a variety of common anions such as Cl−, Br−, NO3−, IO3−, ClO4−, MnO4−, and CrO42−. More importantly, NDTB‐1 is selective for the removal of TcO4− from nuclear waste streams even though there are large excesses of competing anions such as Cl−, NO3−, and NO2−. Competing anion exchange experiments and magic‐angle spinning (MAS)‐NMR spectroscopy of anion‐exchanged NDTB‐1 demonstrate that this unprecedented selectivity originates from the ability of NDTB‐1 to trap TcO4− within cavities, whereas others remain mobile within channels in the material. The exchange kinetics of TcO4− in NDTB‐1 are second‐order with the rate constant k2 of 0.059 s−1 M−1. The anion exchange capacity of NDTB‐1 for TcO4− is 162.2 mg g−1 (0.5421 mol mol−1) with a maximum distribution coefficient Kd of 1.0534 × 104 mL g−1. Finally, it is demonstrated that the exchange for TcO4− in NDTB‐1 is reversible. TcO4− trapped in NDTB‐1 can be exchanged out using higher‐charged anions with a similar size such as PO43− and SeO42−, and therefore the material can be easily recycled and reused.

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Achieving global optimization of inorganic sorbent efficacy, as well as tailoring sorbent specificity for target sorbates would facilitate increased wide-spread use of these materials in applications such as producing potable water or nuclear waste treatment. Sodium titanates have long been known as sorbents for radionuclides;90 Sr and transuranic elements in particular. We have developed a related class of materials, which we refer to as peroxo-titanates: these are sodium titanates or hydrous titanates processing, storing and utilizing the peroxo-titanate as an aqueous slurry rather than a dry powder, and post-synthesis acidification. All three synthesis modifications; addition of hydrogen peroxide, use of a slurry form and acidification can be applied more broadly to the optimization of other metal oxide sorbents and other ion separations processes.

Thioredoxin reductase (TrxR) reduces thioredoxin (Trx), thereby contributing to cellular redox balance, facilitating the synthesis of deoxy-ribose sugars for DNA synthesis, and regulating redox-sensitive gene expression. Auranofin is a gold compound that potently inhibits TrxR. This inhibition is one suspected mechanism of auranofin's therapeutic benefit in the treatment of rheumatoid arthritis. The use of other gold compounds to treat cancer or inflammatory disease may rely on their ability to inhibit TrxR. In the current study, we tested the hypothesis that a variety of gold compounds may inhibit TrxR.Methods: We exposed rat-TrxR1 to auranofin, gold sodium thiomalate, sodium aurothiosulfate, triphenyl phosphine gold chloride, or gold acetate, and measured TrxR activity ex-vivo. We then compared TrxR1 inhibitory levels of gold compounds to those that inhibited mitochondrial activity of THP1 monocytes and OSC2 epithelial cells, estimated by succinate dedhydrogenase activity.Results: All gold compounds inhibited TrxR1 at concentrations ranging from 5-4000 nM (50% inhibitory concentration). The oxidation state of gold did not correlate with inhibitory potency, but ligand configuration was important. Au(I)-phosphine compounds (triphenyl phosphine gold chloride and auranofin) were the most potent inhibitors of TrxR. All TrxR1 inhibitory concentrations were sublethal to mitochondrial activity in both THP1 and OSC2 cells. AbstractThioredoxin reductase (TrxR) reduces thioredoxin (Trx), thereby contributing to cellular redox balance, facilitating the synthesis of deoxy-ribose sugars for DNA synthesis, and regulating redox-sensitive gene expression. Auranofin is a gold compound that potently inhibits TrxR. This inhibition is one suspected mechanism of auranofin's therapeutic benefit in the treatment of rheumatoid arthritis. The use of other gold compounds to treat cancer or inflammatory disease may rely on their ability to inhibit TrxR. In the current study, we tested the hypothesis that a variety of gold compounds may inhibit TrxR.Methods: We exposed rat-TrxR1 to auranofin, gold sodium thiomalate, sodium aurothiosulfate, triphenyl phosphine gold chloride, or gold acetate, and measured TrxR activity ex-vivo. We then compared TrxR1 inhibitory levels of gold compounds to those that inhibited mitochondrial activity of THP1 monocytes and OSC2 epithelial cells, estimated by succinate dedhydrogenase activity.Results: All gold compounds inhibited TrxR1 at concentrations ranging from 5-4000 nM (50% inhibitory concentration). The oxidation state of gold did not correlate with inhibitory potency, but ligand configuration was important. Au(I)-phosphine compounds (triphenyl phosphine gold chloride and auranofin) were the most potent inhibitors of TrxR. All TrxR1 inhibitory concentrations were sublethal to mitochondrial activity in both THP1 and OSC2 cells.Conclusions: Diverse types of gold compounds may be effective inhibitors of TrxR1 at concentrations that do not suppress cellular mitochondrial function. Inhibition may ...