Characterization of iron uptake in the magnetic bacteriumAquaspirillum sp. AMB-1

Applied Biochemistry and Biotechnology - The aim of this work is to elucidate the iron uptake mechanism in the magnetic bacteriumAquaspirillum sp. AMB-1, which can utilize a wide variety of iron...     

Software studies of GLD calorimeter

The baseline design of the GLD calorimeter is scintillator-strip arrays interleaved with absorber plates. We present preliminary performance studies of the hit clustering with this calorimeter using a simulator. Also, simulation results of a ‘digital’ calorimeter, which is an option of the GLD calorimeter, are presented.      

Vesicle disruption, plasma membrane bleb formation, and acute cell death caused by illumination with blue light in acridine orange-loaded malignant melanoma cells

Acridine orange (AO), a weakly basic fluorescent dye, is permeable to plasma and vesicle membranes and preferentially remains in intracellular acidic regions. Using fluorescence microscopy, we observed dynamic changes in AO-loaded cultured malignant melanoma cells during illumination with blue light. Immediately after the start of the illumination, the successive disruption of vesicles was observed as a flash of fluorescence, and shortly after that, blebs were formed on the plasma membrane. These cells died within 5 min. Vesicle disruption was completely inhibited when cells were treated with the vacuolar H(+)-ATPase inhibitor bafilomycin A1 followed by loading with AO, but not when bafilomycin A1 was treated after AO loading. Thus, the filling of AO in the vesicle, which is driven by vacuolar H(+)-ATPase, is initially required for vesicle disruption. In contrast, bafilomycin A1 did not prevent plasma membrane blebbing, indicating that the blebs are formed independently of the vesicle disruption. Acute cell death was inhibited by treatment with bafilomycin A1 before but not after AO loading. Thus, AO- and blue light-induced acute cell death is associated with vesicle disruption rather than bleb formation. Both the vesicle disruption and the formation of plasma membrane blebs were inhibited by removal of oxygen from the cell environment and by singlet oxygen scavengers, sodium azide, ascorbic acid, and L-histidine, but not inhibited by the hydroxyl radical scavenger dimethyl thiourea. Acute cell death was also prevented by singlet oxygen scavengers but not by dimethyl thiourea. Thus, these phenomena are likely caused at least in part by the generation of singlet oxygen. The photosensitive features of plasma and vesicle membranes observed in the present study may be based on the use of the photodynamic effect, such as cancer therapy.     

In situ generation of oxo-sulfidobis(dithiolene)tungsten(VI) complexes: active-site models for the aldehyde ferredoxin oxidoreductase family of tungsten enzymes

Oxo-sulfidobis(dithiolene)tungsten(VI) complexes were prepared in situ by the reaction of oxobis(dithiolene)tungsten(V) precursors with hydrosulfide (SH-). The complexes, characterized by UV-vis, electrospray ionization mass spectrometry, IR, and resonance Raman spectroscopies, model the proposed coordination environment and observed hydrolytic reactions of members of the aldehyde ferredoxin oxidoreductase family of tungsten enzymes.