PubMed · 10692206
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M L Sivilotti. 2000. Methanol intoxication.. https://doi.org/10.1016/s0196-0644(00)70090-4
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Iron cycling and the associated changes in solid phase have dramatic implications for trace element mobility and bioavailability. Here we explore the formation of secondary iron phases during microbially mediated reductive dissolution of ferrihydrite-coated sand under dynamic flow conditions. An initial period (10 d) of rapid reduction, indicated by consumption of lactate and production of acetate and Fe-(II) to the pore water in association with a darkening of the column material, is followed by much lower rate of reduction to the termination of the experiment after 48 d. Although some Fe (<25%) is lost to the effluent pore water, the majority remains within the column as ferrihydrite (20-70%) and the secondary mineral phases magnetite (0-70%) and goethite (0-25%). Ferrihydrite converts to goethite in the influent end of the column where dissolved Fe(II) concentrations are low and converts to magnetite toward the effluent end where Fe(III) concentrations are elevated. A decline in the rate of Fe(II) production occurs concurrent with the formation of goethite and magnetite; at the termination of the experiment, the rate of reduction is <5% the initial rate. Despite the dramatic decrease in the rate of reduction, greater than 80% of the residual Fe remains in the ferric state. These results highlight the importance of coupled flow and water chemistry in controlling the rate and solid-phase products of iron (hydr)oxide reduction.
BACKGROUND: Although statins preserve endothelial function by reducing serum cholesterol levels, it has been suggested they may also stimulate nitric oxide (NO) synthase in endothelium with concurrent increase in superoxide (O2-) generation, leading to impairment of NO activity. Therefore, measurements of biologically active NO and O2- in endothelium after exposure to the HMG-CoA reductase inhibitor cerivastatin were undertaken to evaluate its potential effect on NO biological activity. METHODS AND RESULTS: Highly sensitive electrochemical NO and O2- microsensors were placed near the surface of a single human umbilical vein endothelial cell, and the kinetics of NO and O2- release were recorded in vitro. Cerivastatin demonstrated a time-dependent effect on NO release in endothelial cells. The initial release (approximately the first 3 minutes) was concentration-dependent (0.01 to 10 micromol/L) and was similar to that observed for typical NO synthase agonists calcium ionophore or acetylcholine. Cerivastatin stimulated NO release at a favorable rate and scavenged O2-, which led to the preservation of the active concentration of NO. The sustained effect (after approximately 6 hours) of cerivastatin on endothelium was associated with an approximately 35% increase in NO release as compared with the initial effect. In contrast to the initial effect, the sustained effect of cerivastatin was shown at concentrations approximately 100-fold lower and was dependent on inhibition of endothelial HMG-CoA reductase. CONCLUSIONS: These data provide direct evidence to prove that in the presence of cerivastatin, the NOS system in endothelium operates with high efficiency toward increasing NO activity by activation of NO release and by concurrent inactivation of O2-.
Shewanella putrefaciens, a heterotrophic member of the gamma-proteobacteria is capable of respiring anaerobically on Fe(III) as the sole terminal electron acceptor (TEA). Recent genetic and biochemical studies have indicated that anaerobic Fe(III) respiration by S. putrefaciens requires outer-membrane targeted secretion of respiration-linked Fe(III) reductases. Thus, the availability of Fe(III) to S. putrefaciens may be governed by equilibrium chemical speciation both in the solution phase and at the bacterial cell-aqueous or cell-mineral interface. In the present study, effects of Fe(III) speciation on rates of bacterial Fe(III) reduction have been systematically examined by cultivating S. putrefaciens anaerobically on a suite of Fe(III)-organic complexes as the sole TEA. The suite of Fe(III)-organic complexes spans the range of stability constants normally encountered in natural water systems and includes Fe(III) complexed to citrate, 5-sulfosalicylate, NTA, salicylate, tiron, and EDTA. Rates of bacterial Fe(III) reduction in the presence of dissolved chelating agents correlate with the thermodynamic stability constants of the Fe(III)-organic complexes, implying that chemical speciation governs Fe(III) bioavailability. Equilibrium Fe(III) sorption experiments measured the reversible coordination of Fe(III) with S. putrefaciens as a function of cell/Fe(III) concentration, time, and activity of competing chelating agents. Results show that S. putrefaciens readily sorbs dissolved Fe(III) but that adsorption is restricted by the presence of strong Fe(III)-chelating agents. Our results indicate that dissimilatory Fe(III) reduction by S. putrefaciens is controlled by equilibrium competition for Fe(III) between dissolved organic ligands and strongly sorbing functional groups on the cell surface.