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At least 325 records · Page 18Linked to original sources
PubMed1999

The effects of silver on intestinal ion and acid-base regulation in the marine teleost fish, Parophrys vetulus.

Exposure to elevated silver (as AgNO3) concentrations (6-9 microM) in seawater was associated with comparably high silver concentrations in the intestinal fluids of the lemon sole (Parophrys vetulus), and a tendency for reduced drinking rate. The effects of silver on intestinal ion and acid-base regulation were studied using in situ perfusion of the intestine. Intestinal net Cl- uptake was reduced from 0.4 to 0.1 and intestinal net Na+ uptake from 0.2 to 0 mmol kg(-1) x h(-1) during silver exposure (9 microM). At the same time, intestinal HCO3- net efflux was reduced from 0.2 to 0.1 mmol kg(-1) x h(-1). Both intestinal Na+ and Cl- uptake and Cl-/HCO3- exchange are thus sensitive to silver, but to different extents. None of the observed effects were reversible during 24 h of recovery. Intestinal water transport was highly variable in vivo in the perfused preparation, and no significant effect of silver exposure was observed. However, in vitro intestine preparations exhibited reduction of intestinal net water flux from 4 to 1 microl cm(-2) x h(-1) during silver exposure together with reduced unidirectional Cl- influx. Reduced water intake and transepithelial water transport in silver-exposed fish resulted in moderate hemoconcentration evident from higher hematocrit values, but not in increased plasma ion levels. The latter could reflect a compensatory response via increased branchial Na+/K+-ATPase levels, observed in silver-exposed fish, indicative of increased branchial ion transport capacity. Impairment of intestinal ion and water transport as a result of silver intake via drinking could be an important part of the fatal cascade of physiological effects observed in marine fish during acute silver exposure.

Acid-Base Equilibrium↗
PubMed2005

Development and testing of a silver chloride-impregnated activated carbon for aqueous removal and sequestration of iodide.

Silver impregnated activated carbon (SIAC) can effectively remove iodide from water and sequester it in the form of AgI(s)). Given the extremely insoluble nature of AgI(s), the spent SIAC can be safely disposed of in land burial facilities. However, when the molar ratio of silver to iodide is greater than one, which is typical for waters contaminated with iodide, unreacted silver on the SIAC leached into solution with decreasing pH. To minimize silver leaching, a silver chloride impregnated activated carbon (SIAC-Cl) was produced from a SIAC. Scanning electron microscopy (SEM), energy-dispersive X-ray (EDX) and X-Ray Diffraction (XRD) analyses confirmed the presence of silver chloride on the SIAC-Cl. Batch isotherm experiments conducted at pH 5, 7 and 8 showed that the iodide uptakes of SIAC-Cl and SIAC were similar and independent of pH. SEM/EDX and XRD analyses after reaction with iodide indicated that chloride was exchanged with iodide to form AgI(s) on the SIAC-Cl. Batch leaching experiments demonstrated that leaching of silver from SIAC-Cl under acidic conditions was significantly lower than from SIAC. The performance of SIAC and SIAC-Cl for practical applications was evaluated by conducting column experiments using a radioactively contaminated groundwater that included 129I. SIAC and SIAC-Cl showed similar degrees of iodide uptake. However, a significant degree of silver leaching, about 50% of the total silver, occurred from the SIAC during the course of the column experiments, whereas silver leaching from SIAC-Cl was remarkably low (only 6% of the total silver). SIAC-Cl appears to be a suitable getter material to remove and sequester iodide from contaminated waste streams.

Adsorption↗
PubMed1995

Location of focal silver staining at endothelial gaps in inflamed venules examined by scanning electron microscopy.

The century-old histological technique of silver nitrate staining has proven to be extremely useful for visualizing endothelial cell borders and localizing endothelial gaps, but the significance of the staining is still not fully understood. To gain some insight into what silver nitrate stains, we developed a method that enabled us to use scanning electron microscopy with backscattered and secondary electron imaging to examine silver staining at endothelial cell borders of venules of the rat tracheal mucosa. We found that in normal venules, silver lines followed the smooth contour of cell borders. However, 1 min after endothelial permeability was increased by substance P, cell borders were irregular and displaced from the silver lines by as much as 4.3 microns, and the lines were accompanied by three types of silver deposits. Most common (46% of total) were annulus-shaped silver deposits that surrounded endothelial gaps. These deposits averaged 1.5 microns in width, were positioned symmetrically across cell borders, and were located at a depth of 0.3 micron beneath the luminal surface. Many endothelial gaps were partitioned into multiple pores (mean, 2.4) by fingerlike processes of endothelial cells. Surprisingly, the gaps occupied only 5.4% of the total area of the silver deposits and constituted 0.15% of the luminal surface of the leaky postcapillary venules. A second type of silver deposit (19% of total) was positioned asymmetrically with respect to the cell border and marked sites where endothelial cell margins still overlapped but appeared to be vertically separated by obliquely oriented gaps. A third type marked gaps at three-cell junctions; these were no more abundant than deposits elsewhere around the cell perimeter, suggesting that three-cell junctions were not unusually leaky sites. We conclude that silver nitrate marks endothelial cell borders and outlines endothelial cell gaps by staining an element of intercellular junctions. The annular shape of many silver deposits around gaps suggests that junctional elements in the apposing cells are separated during gap formation but are still present at the gap perimeter.

Animals↗
PubMed2004

Time course analysis of the mechanism by which silver inhibits active Na+ and Cl- uptake in gills of rainbow trout.

A time course analysis using (110m)Ag, (24)Na(+), and (36)Cl(-) examined gill silver accumulation and the mechanism by which waterborne silver (4.0 x 10(-8) M; 4.3 microg/l) inhibits Na(+) and Cl(-) uptake in gills of freshwater rainbow trout. Analyses of gill and body fluxes allowed calculation of apical uptake and basolateral export rates for silver, Na(+), and Cl(-). To avoid changes in silver bioavailability, flow-through conditions were used to limit the buildup of organic matter in the exposure water. For both Na(+) and Cl(-) uptake, apical entry, rather than basolateral export, was the rate-limiting step; Na(+) and Cl(-) uptake declined simultaneously and equally initially, with both uptakes reduced by approximately 500 nmol.g(-1).h(-1) over the 1st h of silver exposure. There was a further progressive decline in Na(+) uptake until 24 h. Carbonic anhydrase activity was inhibited by 1 h, whereas Na(+)-K(+)-ATPase activity was not significantly inhibited until 24 h of exposure. These results indicate that carbonic anhydrase inhibition can explain the early decline in Na(+) and Cl(-) uptake, whereas the later decline is probably related to Na(+)-K(+)-ATPase blockade. Contrary to previous reports, gill silver accumulation increased steadily to a plateau. Despite the rapid inhibition of apical Na(+) and Cl(-) uptake, apical silver uptake (and basolateral export) increased until 10 h, before decreasing thereafter. Thus silver did not inhibit its own apical uptake in the short term. These results suggest that reduced silver bioavailability is the mechanism behind the pattern of peak and decline in gill silver accumulation previously reported for static exposures to silver.

Algorithms↗
PubMed1999

Mechanism of branchial apical silver uptake by rainbow trout is via the proton-coupled Na(+) channel.

The branchial uptake mechanism of the nonessential heavy metal silver from very dilute media by the gills of freshwater rainbow trout was investigated. At concentrations >36 nM AgNO(3), silver rapidly entered the gills, reaching a peak at 1 h, after which time there was a steady decline in gill silver concentration and a resulting increase in body silver accumulation. Below 36 nM AgNO(3), there was only a very gradual increase in gill and body silver concentration over the 48-h exposure period. Increasing water sodium concentration ([Na(+)]; 0.05 to 21 mM) significantly reduced silver uptake, although, in contrast, increasing ambient [Ca(2+)] or [K(+)] up to 10 mM did not reduce silver uptake. Kinetic analysis of silver uptake at varying [Na(+)] showed a significant decrease in maximal silver transport capacity (173 +/- 34 pmol. g(-1). h(-1) at 0.1 mM [Na(+)] compared with 35 +/- 9 at 13 mM [Na(+)]) and only a slight decrease in the affinity for silver transport (K(m); 55 +/- 27 nM at 0.1 mM [Na(+)] compared with 91 +/- 47 nM at 13 mM [Na(+)]). Phenamil (a specific blocker of Na(+) channels), at a concentration of 100 microM, blocked Na(+) uptake by 78% of control values (58% after washout), and bafilomycin A(1) (a specific blocker of V-type ATPase), at a concentration of 2 microM, inhibited Na(+) uptake by 57% of control values, demonstrating the presence of a proton-coupled Na(+) channel in the apical membrane of the gills. Phenamil (after washout) and bafilomycin A(1) also blocked silver uptake by 62 and 79% of control values, respectively, indicating that Ag(+) is able to enter the apical membrane via the proton-coupled Na(+) channel.

Amiloride↗
PubMed1998

Indentation creep behavior of a direct-filling silver alternative to amalgam.

Amalgam creep has been identified as a key parameter associated with marginal breakdown and corrosion. The aim of this study was to evaluate the time-dependent deformation (creep) of a novel silver filling material as an alternative to amalgam. We made the silver specimens by pressing a precipitated powder at room temperature to a density that can be achieved in clinical hand consolidation. The surface of the silver was either polished or burnished. To examine local contact creep and the effect of surface finishing, we used an indentation creep method in which a Vickers indenter was loaded on the specimen surface at a load of 10 N with dwell times of 5 sec to 6x10(4) sec. We used a bonded-interface technique to examine subsurface creep mechanisms. The flexural strength (mean+/-SD; n = 10) was 86+/-20 MPa for amalgam, 180+/-21 MPa for polished silver, and 209+/-19 MPa for burnished silver-values which are significantly different from each other (family confidence coefficient = 0.95; Tukey's multiple-comparison test). Indentation creep manifested as hardness number decreasing with increased dwell time. With dwell time increasing from 5 sec to 6x10(4) sec, the hardness number of amalgam was reduced by approximately 80%; that of the polished silver and the burnished silver was reduced by only 40%. Subsurface creep in amalgam consisted of the shape change of the alloy particles from spherical to elongated shapes, and the separation of matrix grains from each other, possibly due to grain-boundary sliding. Creep of the polished silver occurred by densification reducing porosity and increasing hardness; that of the burnished silver occurred by the displacement of the burnished layer. These results suggest that, due to creep-induced subsurface work-hardening and densification, the consolidated silver exhibits a higher resistance to indentation creep than does amalgam. The hardness number of silver approaches that of amalgam after prolonged indentation loading.

Analysis of Variance↗
PubMedDate not supplied

Application of silver degeneration stains for neurotoxicity testing.

Silver staining procedures have been used in numerous ways to render a variety of physical and biological features visible. In biological tissue, histologic protocols use silver to visualize diverse structures or features, such as reticulin, melanin, fungi, chromosome bands, nucleolar organizing regions, and different features in the nervous system. A comparison of the specific steps in these protocols indicates that the silver is "directed" to stain any given feature by the type of fixation, the pretreatment ("mordanting"), the composition of the silver-containing solution(s), and the form of development (reduction). Since the mechanisms of staining have not been understood historically (nor are they now), each method was developed by trial and error. Keystone methods such as those of Bodian and Bielschowsky exploit the nervous system's affinity for silver (argyrophilia). The beginning of a new era in brain research came with the recognition that distinct silver-impregnated morphologic changes occurring in damaged axons could be used for tracing axon pathways in experimental animals with specifically placed lesions. Improvements in staining methods used to selectively impregnate the disintegrating axons but to leave normal axons unstained were achieved by Nauta and Gygax (early workers with these procedures) and spawned a host of method variations known as the "Nauta" methods. Of these, the Fink-Heimer and de Olmos cupric-silver methods were able to unambiguously demonstrate disintegrating synaptic terminals, thereby allowing complete tracing of axon pathways. The late 1970s and 1980s witnessed innovative applications of these techniques. The silver methods once used to trace axon pathways became indicators of the extreme endpoint of neurotoxicity: disintegrative degeneration of neurons induced by neurotoxic chemicals that were administered systemically. The hallmark of neurotoxic substances is the selectivity with which each destroys specific populations or subpopulations of neurons. The high contrast and sensitivity of the silver degeneration stains greatly facilitate the screening process to detect these affected populations, especially when there is no basis for knowing where in the brain to look for damage. More recently, in addition to expanded use in screening for neurotoxic effects, the silver degeneration stains are being used to chart the neuron populations undergoing programmed cell death in the developing brain. Other newly developed silver methods have been refined to show nondisintegrative degeneration, such as the plaques,and tangles of Alzheimer's disease.

Animals↗
PubMed1983

A silver method for counterstaining plastic embedded tissue.

This report presents a method which can be used for counterstaining semithin sections of plastic embedded tissue. The sections are treated with a solution of silver lactate, followed by physical development. During the silver lactate treatment, silver ions are bound by various tissue components as metallic silver or silver sulfide. During physical development catalytic reduction of silver ions to metallic silver takes place where silver has been bound in the tissue, enlarging the silver deposits to microscopically visible dimensions. The amplified silver deposits give high contrast staining in yellow, brown and black suitable for both color and monochrome photography. The localization of the silver deposits is highly specific and may reflect several independent chemical processes. Examples in several tissues are shown.

Animals↗
PubMed1999

[Transmission electron microscopic observations on dentin structures stained with silver].

The purpose of this study was to investigate the ultrastructure of silver deposit regions on human dentin. Three kinds of silver stained specimens were used in this study, the decalcified celloidin section stained with silver, the frozen section of decalcified tooth stained with silver, and the decalcified section of undecalcified tooth treated by the silver iontophorese method. After light microscopic observation of the specimens, these were embedded again in epoxy resin and ultra thin sections were made. Then these ultra thin sections were observed under transmission electron microscope, and the results were as follows: 1. By observing the decalcified celloidin section stained with silver, a deposition of silver particles was found on the surface and inside of the hypocalcified collagen fibrils. 2. By observing the section of decalcified tooth stained with silver, a deposition of silver particles was found on the hypercalcified collagen fibrils. According to the findings, it was concluded that the interglobular net and the dark-line of mineralized striation in dentin are hypercalcified regions. 3. By using the silver iontophorese method, large silver particles were found deposited among the hypocalcified collagen fibrils. 4. It was confirmed that the degree of mineralization of collagen fibrils in hard tissue can be estimated indirectly observing the morphological change of collagen fibrils in a decalcified section.

Collagen↗
PubMed1990

An experimental study on silver in the nervous system and on aspects of its general cellular toxicity.

Exposure of foetal and adult rats to silver results in a long-lasting deposition of the metal in many structures of the nervous system. A brief anatomical description of the localization of silver deposits as they are visualized by autometallography is provided. The consequences of silver in the nervous system were evaluated by volumetric measurements on developing rat hippocampi which showed that silver induced a decrease in the total volume of hippocampal pyramidal cells. The toxicity of silver at the cellular level was studied in a test-system of cultured macrophages. High doses of silver caused coagulation necrosis, whereas lower concentrations resulted in a cytotoxic and possibly a cytostatic effect without affecting cell structure. The processing of silver which resulted in lysosomal accumulations was affected by the metal itself in a dose-dependent fashion (autointerference). Other basic macrophage functions (protein-production, phagocytosis, migration) were not affected by silver at concentrations which did not cause acute cell death. Biochemically, silver causes an increase in lipid peroxidation, which was evident only in liver tissue. Coagulation necrosis and, to some extent, long-term effects on cell viability could be reversed by inorganic selenium, which was tested as a detoxicant. On the other hand, pre-exposure of animals to selenium greatly enhanced the silver-induced lipid peroxidation. Furthermore, the co-exposure to silver and nickel resulted in a synergistically increased lipid peroxidation.

Animals↗
PubMed1987

Serum and urinary silver levels in thermal injury patients.

Although silver sulfadiazine has been used extensively as an effective topical antimicrobial agent in thermal injury patients, little is known about the cutaneous absorption of the silver moiety in these patients. Therefore, we longitudinally evaluated both serum silver concentration and 24-hour urinary excretion of silver in 23 patients with second- and third-degree thermal burns. Mean serum silver concentrations were modestly elevated throughout the patients' hospital course. Urinary excretion of silver was markedly elevated, especially in those patients with more severe burns. Indeed, in patients who had burns covering more than 60% of the total body surface area mean peak silver excretion was 1100 micrograms/24 hr (normal, less than 1 micrograms/24 hr). Thus, silver ion is absorbed across the burn wound in thermal injury patients treated with silver sulfadiazine. The 24-hour urinary excretion of silver appears to be a very sensitive indicator of cutaneous absorption in these patients. Possible implications of this cutaneous silver absorption warrant further evaluation.

Administration, Topical↗
PubMed2006

Controlled synthesis of double- and multiwall silver nanotubes with template organogel from a bolaamphiphile.

Double- and multiwall silver nanotubes were synthesized by using the uniform low-molecular-mass organogel nanotubes self-assembled from an L-glutamic-acid-based bolaamphiphile, N,N-eicosanedioyl-di-L-glutamic acid (EDGA). The EDGA could gel a mixed water/ethanol solvent and form helical nanotubes. When the gel thus formed was mixed with AgNO3 in water/ethanol, the silver(I) cations could be coordinated with both the inner and outer surfaces of the EDGA nanotubes. The reduction of the silver cation under the photoirradiation yielded double-wall silver nanotubes, where two silver layers were separated by one EDGA layer. Elongations of the reduction time of the mixed gels and AgNO3 in the solution lead to the formation of three-, four-, and five-wall silver nanotubes. In these multiwall silver nanotubes, each wall was separated at a distance of about 2.7 nm, which was just the molecular length of the bolaamphiphile. It was suggested that the dissolved EDGA molecules and excess Ag(I) cations were further assembled onto the surface of the formed double-wall silver nanotubes and, as a consequence, the photoreduction caused the formation of the third-wall silver nanotubes. The multiwall silver nanotubes were further formed in a similar way. The factors affecting the formation of the silver wall nanotubes such as the relative amount of AgNO3 to EDGA and the synthetic conditions were discussed.

Journal Article↗
PubMed2004

Novel method for preparing controllable and stable silver particle films for surface-enhanced Raman scattering spectroscopy.

A new surface-enhanced Raman scattering (SERS) active substrate has been developed based on our previous study. Small silver nanoparticles on a quartz slide can be enlarged by using a mixture of commercially available reagents called Silver Enhancer and Initiator. The optical properties and characteristics of the new substrate have been investigated by ultraviolet-visible (UV-Vis) spectroscopy and atomic force microscopy (AFM). The results indicate that the small silver nanoparticles grow and some silver aggregates emerge on the quartz slide after the slide is immersed into the Silver Enhancer and Initiator Mixture (SEIM). The average diameter of the silver nanoparticles on the substrate becomes approximately double after the immersion into SEIM for 20 s. 1,4-bis[2-(4-pyridyl)ethenyl]-benzene (BPENB) was used as a Raman probe to evaluate the enhancement ability of the new silver substrate. It has been found that the SERS intensity can be increased about 10 times by using the substrate treated by SEIM compared with that without being treated by SEIM. Interestingly enough, the SERS enhancement increases with time. This may be due to the reorganization of silver nanoparticles on the quartz surface. The new substrate can remain active for more than 90 days. The adsorption mode of BPENB on the new substrate and the dependence of the BPENB configurations on the concentration of BPENB in methanol solution have also been investigated by SERS or UV-Vis spectroscopy. The SERS spectra of a self-assembled monolayer (SAM) BPENB film adsorbed on a silver substrate treated by SEIM show that BPENB molecules are chemically absorbed through the Ag-N bond. Consequently, a nearly perpendicular orientation of BPENB on the silver surface is proposed. The SERS spectra of BPENB SAMs on the new substrates fabricated from methanol solutions with different concentrations are compared. The concentration dependence of the SERS spectra reveals that the BPENB molecules are adsorbed on the silver film as monomers when the film is prepared from the solution with a lower concentration (<4 x 10(-6) M) and as aggregates when it is prepared from the solution with a higher concentration (>1 x 10(-5) M).

Journal Article↗
PubMed1988

Therapeutic effects of silver nylon dressings with weak direct current on Pseudomonas aeruginosa-infected burn wounds.

The therapeutic and prophylactic effects of nylon dressings coated with metallic silver in a direct current circuit have been examined in a rat model of fatal burn wound sepsis. Male Sprague-Dawley rats weighing 325 +/- 25 grams with 20% full-thickness scald injuries were used. Therapeutic effects were examined at 4 or 24 hours after surface inoculation with a lethal dose of Pseudomonas aeruginosa (Strain 59-1244). When used as a surface anode with an implanted silver needle cathode, the silver nylon was therapeutic at currents between 0.4 and 40 microA when applied at either test time and continued for 5 days (p less than 0.001). When used as a cathode, silver nylon was not effective. Nylon cloth without a silver metal coating was not effective without applied current or when used as an anode. Silver nylon dressings placed at 4 hours after inoculation but without applied current showed significant effectiveness (p less than 0.01). This effect, however, was significantly less than that seen with silver nylon used as an anode (p less than 0.001). Barrier prophylactic effects were examined by placing silver nylon or uncoated nylon on burn wounds before inoculation with Pseudomonas aeruginosa. The uncoated nylon had no barrier effect. Silver nylon was found protective but applied current was not required for significant (p less than 0.001) barrier effect. These results indicate silver nylon dressings may be a valuable antimicrobial burn wound covering device.

Animals↗
PubMed2006

Silver-coated dressing acticoat caused raised liver enzymes and argyria-like symptoms in burn patient.

BACKGROUND: Treatment of acute burn wounds with silver sulfadiazine (SSD) has raised concern about potential silver toxicity. Numerous adverse reactions and side effects have been reported and an increasing resistance to SSD, especially in Pseudomonas strains, have motivated researchers to search for an alternative wound dressing. METHODS: Recently, a silver-coated wound dressing Acticoat (Smith & Nephew, Inc.) has become available for use in burn patients. It is a three-ply dressing, consisting of an inner rayon/polyester absorptive core between two layers of silver-coated, high-density polyethylene mesh. In a moist environment, the nanocrystals of silver are released and improve the microbial control in the wound. RESULTS: After 1 week of local treatment with Acticoat in a young, previously healthy 17-year-old boy with 30% mixed depth burns, hepatotoxicity and argyria-like symptoms, a grayish discoloration of the patient's face, appeared. The silver levels in plasma (107 microg/kg) and urine (28 microg/kg) were clearly elevated, as well as the liver enzymes. As soon as the local application of Acticoat was aborted, the clinical symptoms and liver enzymes returned to the normal values. CONCLUSIONS: This is the first report on silver toxicity in a patient with 30% burns who received Acticoat for local treatment. Due to substantial experiences with adverse SSD reactions and side effects, it is appropriate to keep the possibility of a toxic silver effect in burn patients treated with Acticoat silver-coated wound dressing in mind. The silver levels in plasma and/or urine should be monitored.

Adolescent↗
PubMed2006

Influence of salinity and organic carbon on the chronic toxicity of silver to mysids (Americamysis bahia) and silversides (Menidia beryllina).

Tests were conducted with mysids (Americamysis bahia) and silversides (Menidia beryllina) to evaluate the influence of salinity and organic carbon on the chronic toxicity of silver. During 7- and 28-d tests conducted at 10, 20, and 30% per hundred salinity, higher concentrations of dissolved silver generally were required to cause a chronic effect as the salinity of the seawater was increased. The 28-d mysid and silverside 20%-effective concentration values (expressed as dissolved silver) ranged from 3.9 to 60 and from 38 to 170 microg/L, respectively, over the salinity range. This pattern was not observed when the same test results were evaluated against the concentrations of free ionic silver (measured directly during toxicity tests), as predicted by the free-ion activity model. Increasing the concentration of dissolved organic carbon from 1 mg/L to the apparent maximum achievable concentration of 6 mg/L in seawater caused a slight decrease in chronic toxicity to silversides but had no effect on the chronic toxicity to mysids. The possible additive toxicity of silver in both food and water also was investigated. Even at the maximum achievable foodborne concentration, the chronic toxicity of silver added to the water was not affected when silver was also added to the food, based on the most sensitive endpoint (growth). However, although fecundity was unaffected at all five tested concentrations during the test with silver in water only, it was significantly reduced at the two highest waterborne silver concentrations (12 and 24 microg/L) during the test with silver dosed into food and water.

Animals↗
PubMed2002

Silver activates calcium signals in rat basophilic leukemia-2H3 mast cells by a mechanism that differs from the Fc epsilon RI-activated response.

We previously showed that silver stimulates degranulation and leukotriene (LT) C(4) production in rat basophilic leukemia mast cells and now show that silver induces these events by a mechanism that differs from the FcepsilonRI-mediated response. In common with FcepsilonRI cross-linking, silver induced tyrosine phosphorylation of extracellular signal-regulated kinases and furthermore, PD98059, a specific inhibitor of extracellular signal-regulated kinase kinase dose-dependently inhibited the silver-induced LTC(4) production. In contrast to FcepsilonRI cross-linking, silver had no effect on the production of IL-4 and TNF-alpha, indicating that different mechanisms are involved in the activation by these two stimuli. In line with this, silver had no or only marginal effect on the tyrosine phosphorylation of FcepsilonRIbeta, Lyn, Syk, and linker for activation of T cells, the early and crucial events in FcepsilonRI signaling. Silver induced calcium signals that were involved in the metal-induced degranulation, but not LTC(4) production. Unlike Ag, the silver-induced calcium signals were resistant to the depletion of thapsigargin-sensitive calcium stores and the inhibition of tyrosine kinases and phospholipase Cgamma. These findings indicate that silver activates mast cells by bypassing the early signaling events required for the induction of calcium influx. Our data strongly suggest the existence of an alternative pathway bypassing the early signaling events in mast cell activation and indicate that silver may be useful for analyses of such alternative mechanisms.

Animals↗
PubMed1981

Distribution of silver in the eyes and plasma proteins of the albino rat.

Albino rats were given a 0.25% solution of silver nitrate to drink for 10 weeks, then were divided into two groups. One group continued to drink the solution for an additional 6 months, while the other group was given water to drink for an additional 12 months. The ingestion of silver nitrate retarded the growth of the rats and eventually caused their death. The rats regained weight and appeared to grow normally when the silver nitrate regimen was withdrawn. Radioactive silver in the plasma was found to be almost exclusively in a single electrophoretic protein band. Examination of the rats' eyes by electron microscopy showed deposits of silver particles in Bruch's membrane, the basement membranes of the choriocapillaris and the ciliary processes, and the stroma of the choroid and ciliary processes. The number and size of the particles increased with continued ingestion of silver but decreased if the silver regimen was withdrawn after the initial 10 weeks of ingestion. Fine particles of silver were still present 12 months after the end of the ingestion of silver nitrate. At no time were silver particles seen in the basement membranes or endothelial cells of the retinal capillaries or within the cytoplasm of the pigment epithelium or the epithelial cells of eh ciliary processes.

Animals↗