Lichenoid reactions to gold from dental restorations and exposure to gold through intracoronary implant of a gold-plated stent.
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Dental Restoration, Permanent↗
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Observations on replanted teeth plated with gold foil; reaction to pure gold; mode of epithelial attachment to gold; expulsion of foreign bodies from pockets.
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Bone Plates↗
A comparison of tissue gold levels in guinea-pigs after treatment with myocrisin injected intramuscularly and triethylphosphine gold chloride and myocrisin administered orally.
A comparative study of tissue gold levels produced in guinea-pigs after the oral administration of either triethylphosphine gold chloride or Myocrisin (sodium aurothiomalate) or after the injection of Myocrisin intramuscularly is reported. Gold concentrations were determined 5, 24 and 168 hours after administration in stomach, small intestine, large intestine, kidney, liver and spleen and 5 and 24 hours after administration in skin, adrenals, heart, lung and brain. In gastrointestinal tissues, tissue gold concentrations were highest with triethylphosphine gold chloride. The stomach gold level 5 hours after oral administration of triethylphosphine gold chloride is particularly high and, taken in conjunction with the other gastrointestinal gold levels measured, suggests that a stomach rather than an intestinal absorption mechanism may predominate. A more extensive time-course study on kidney and liver is reported and the possible relationship between tissue concentration and toxicity is discussed.
Administration, Oral↗
Measurement of 'free' gold in patients receiving disodium aurothiomalate and the association of high free to total gold levels with toxicity.
Serum from patients with rheumatoid arthritis (RA) receiving disodium aurothiomalate was analysed for total gold by atomic absorption spectrometry and for unbound (free) gold by the same method after ultrafiltration by an inert membrane. It was shown that it is possible to obtain reliable free gold concentrations by this method. Good correlations were shown between total and 'free' gold and between total and protein bound gold (PBG) for 54 patients with RA who were stabilised on gold therapy. Significant correlation was also shown between the same parameters for a second group of 15 patients starting gold therapy who were bled at weekly intervals for nine weeks immediately before medication. A single correlation with regression for all patients studied again showed good correlation between total and free gold and between total and PBG. Of the 189 paired values plotted, 182 fell within 2SD of the regression lines for the two plots. Of the seven patients with results outside 2SD of the regression line, six presented with side effects during the study.
Arthritis, Rheumatoid↗
Comparison of two dosage schedules of gold salts in the treatment of rheumatoid arthritis. Relationship of serum gold levels to therapeutic response.
Two doses of gold sodium thiomalate were compared for their effect on rheumatoid arthritis. Thirty-seven patients with active disease for longer than 6 months were treated with 25 mg of gold sodium thiomalate for an average of 29.6 weeks, then at biweekly or monthly intervals to complete 2 years of treatment. Thirty-eight patients were given more than twice as much gold salt at the same intervals on a flexible dose schedule that produced serum gold levels which averaged 332 microgram/dl during the weekly injection phase. No differences were observed in the therapeutic responses of the two groups. Therefore the minimal dose of gold sodium thiomalate required to induce a response in rheumatoid arthritis is 25 mg or less per week. Serum gold levels in the steady state varied between 95 and 386 microgram/dl and were not related to response. Serum half-life for gold was calculated for patients who had an excellent response and for those who were treatment failures. The rate at which gold disappeared from serum was not related to therapeutic responses.
Adolescent↗
In vivo binding and uptake of low-density lipoprotein-gold- and albumin-gold conjugates by parenchymal and sinusoidal cells of the fetal rat liver.
To elucidate the participation of fetal rat liver cells in the receptor-mediated internalization of low-density lipoproteins (LDL), rat fetuses were injected with either LDL-gold or albumin-gold conjugates. The degree of binding and uptake of LDL-gold and albumin-gold by parenchymal and sinusoidal cells of the fetal rat liver differs markedly. Endothelial cells exhibit low LDL-gold uptake. In contrast, parenchymal cells internalize LDL-gold more actively (45 +/- 8 LDL conjugates/100 micrometers2 cytoplasm within 60 min). Kupffer cells exceed this value by a factor of 20. The uptake of albumin-gold by endothelial and Kupffer cells is high, whereas it is extremely low in parenchymal cells. Estradiol pretreatment causes a significant doubling (p less than 0.05) of the LDL-gold particle density/100 micrometers2 cytoplasm both in parenchymal and Kupffer cells, whereas estradiol has no effect on the albumin uptake. The results strongly indicate that LDL uptake by parenchymal and Kupffer cells in the fetal rat liver is mediated by estrogen-inducible receptors, which may correspond to B, E receptors in the adult liver.
Animals↗
Blood gold concentrations in children with juvenile rheumatoid arthritis undergoing long-term oral gold therapy.
During an uncontrolled, open-labelled, open-ended clinical trial of auranofin in children with juvenile rheumatoid arthritis (JRA) we obtained serial blood samples for the purpose of assessing gold content. Our objectives were (1) to observe the pattern of blood gold concentrations over a period of time in children undergoing long-term oral gold therapy, and (2) to observe the effect of changing dosage levels on blood gold concentrations. The initial dosage of auranofin was 0.1 mg/kg/day with allowable increases to 0.2 mg/kg/day. A concurrent nonsteroidal anti-inflammatory drug was allowed. Twenty-one patients were enrolled in the study, and we obtained 2 or more serial samples on 13 of the children. At a constant dosage of 0.1 mg/kg/day, steady state blood gold concentrations were attained in 11 to 13 weeks of therapy and, in the absence of a dosage change, remained remarkably constant through extended periods. The blood gold concentration was related to total daily dosage rather than to the cumulative amount of gold received. Increasing or decreasing the dose resulted in a direct effect on concentration. The clinical value of blood gold levels resulting from auranofin therapy in JRA will have to be established through double-blind controlled trials.
Adolescent↗
Synthesis of luminescent gold(I) and gold(III) complexes with a triphosphine ligand.
We have synthesized and characterized a series of trinuclear gold(I) complexes [(AuX)(3)(mu-triphos)] (triphos = bis(2-diphenylphosphinoethyl)phenylphosphine; X = Cl 1, Br 2, I 3, C(6)F(5) 4) and di- and trinuclear gold(III) complexes [[Au(C(6)F(5))(3)](n)(mu-triphos)] (n = 2 (5), 3 (6)). The crystal structure of 6 [[Au(C(6)F(5))(3)](3)(mu-triphos)] has been determined by X-ray diffraction studies, which show the triphosphine in a conformation resulting in very long gold-gold distances, probably associated with the steric requirements of the tris(pentafluorophenyl)gold(III) units. Complex 6 crystallizes in the triclinic space group P(-1) with a = 12.7746(16) A, b = 18.560(2) A, c = 21.750(3) A, alpha = 98.215(3) degrees, beta = 101.666(3) degrees, gamma = 96.640(3) degrees, and Z = 2. Chloride substitutions in complex 1 afford trinuclear gold(I) complexes [(AuX)(3)(mu-triphos)] (X = Fmes (1,3,5-tris(trifluoromethyl)phenyl) 7, p-SC(6)H(4)Me 8, SCN 9) and [Au(3)Cl(3)(-)(n)()(S(2)CNR(2))(n)(mu-triphos)] (R = Me, n = 3 (10), 2 (12), 1 (14); R = CH(2)Ph, n = 3 (11), 2 (13), 1 (15)). The luminescence properties of these complexes in the solid state have been studied; at low temperature most of them are luminescent, including the gold(III) derivative 6, with the intensity and the emission maxima being clearly influenced by the nature and the number of the ligands bonded to the gold centers.
Journal Article↗
Protein G-gold complex: comparative evaluation with protein A-gold for high-resolution immunocytochemistry.
We combined the protein G-gold complex with several polyclonal and monoclonal antibodies for localization of various antigenic sites. The labelings were compared with those obtained using the protein A-gold complex. The results from either the immunodot experiment or immunoelectron microscopy have demonstrated that, for rabbit and guinea pig antibodies, both protein G-gold and protein A-gold complexes label several different specific antibodies with similar efficiency. However, with antibodies raised in goats or in mice, and particularly with mouse monoclonal antibodies, protein G-gold yielded intense and specific labeling, whereas protein A-gold yielded intense and specific labeling, whereas protein A-gold was very variable; it either gave weaker signals or failed to reveal any specific site or, as with one monoclonal, both protein G and protein A gave similar results. The higher affinity and versatility of protein G over protein A, established by the immunochemical approach, was confirmed by immunocytochemistry. Because of its enhanced reactivity with monoclonal antibodies and its broader affinity for polyclonal antibodies, protein G-gold complex appears to be a better and more versatile probe for high-resolution immunocytochemistry.
Amylases↗
Comparative pharmacokinetics of triethylphosphine gold (auranofin) and gold sodium thiomalate (GST).
The pharmacokinetics of gold sodium thiomalate (GST) and triethylphosphine gold (auranofin; AF) are different. Gold sodium thiomalate (GST) is completely bioavailable while only 15-25% of auranofin (AF) is absorbed. Protein binding of AF occurs to a larger extent to macroglobulins than does GST and total body retention of GST is much greater than AF at six months (30% versus approximately 1%). While terminal serum half-lives are approximately equal, total body half-lives are 250 days for GST and 69 days for AF. In addition, excretory pathways contrast markedly, with 85% of AF appearing in the feces while only 30% of GST is excreted by this route; 15% of AF gold appears in the urine and approximately 70% of GST gold is excreted via this route. With all the above differences one would expect that organ and cellular distribution of these compounds would differ. While gold from both drugs is concentrated in kidney, the percent of the dose found in the kidneys is less for AF than GST, at least in animals (0.4% vs 4.8%). Minute quantities are found in other organs but more study is needed to more clearly define organ distribution of these gold compounds, particularly in man.
Absorption↗
Regional and subcellular distribution of gold in brain of gold thioglucose obese mouse.
By employing neutron activation analysis, endogenous content of gold was estimated quantitatively in discrete brain areas and in subcellular fractions of the hypothalamus of gold thioglucose (GTG) induced obese mice. The highest concentration of gold was obtained in the ventromedial hypothalamus (VMH) reaching approximately 100 ng/mg wet tissue. Significantly higher concentrations were observed in other hypothalamic subareas followed by certain limbic areas and the thalamus, while in the cerebral and the cerebellar cortex the gold concentration was very low. Subcellularly, the hypothalamic gold was principally recovered in the supernatant fraction particularly after a hyposmotic shock treatment of the crude mitochondrial fraction. Contrary to GTG, treatment with gold thiomalate (GTM) did not induce obesity in the mouse, although considerable amount of gold was observed in the VMH, a finding suggesting the existence in the VMH of at least a two step mechanisms for inducing GTG obesity. To identify the satiety neuron transmitter, an analysis of certain enzyme activities involved in the synthesis of known transmitters, such as acetylcholine or gamma-aminobutyric acid (GABA), was made in the GTG-obese mice. There were no significant changes in any of the areas functionally related to the VMH.
Animals↗
Gold kinetics under long-term treatment with gold(I) disodium thiomalate: a comparison in three different mouse strains.
Following weekly i.m. injections of gold(I) disodium thiomalate (GST), mice of strains A.SW and C57BL/6 develop adverse immune reactions, whereas DBA/2 mice do not. We have studied the pharmaco-toxicokinetics of gold in these strains under chronic GST treatment. Our results indicate that the susceptible strains A.SW and C57BL/6 accumulate significantly higher gold concentrations in the liver and spleen compared to the resistant strain DBA/2. In the kidney of DBA/2 mice, gold concentrations persisted at a plateau level, whereas in A.SW and, particularly, C57BL/6 mice early peaks of gold concentrations were followed by a transient decrease, suggestive of tubular toxicity. Whereas splenic T and B cells failed to contain measurable gold concentrations in all three strains, splenic and peritoneal macrophages contained relatively high levels, more so in the susceptible strain C57BL/6 than in the resistant DBA/2 strain. This finding is consistent with the concept that macrophages play an important role in both the adverse and the beneficial effects of gold drugs.
Animals↗
Distribution of gold in rat blood after intravenous administration of auranofin, gold sodium thiomalate and aurothioglucose to rats.
Serum, blood and cell-associated gold were determined at various time periods after intravenous administration of 1 mg Au/kg of auranofin (AF), gold sodium thiomalate (GSTM) and aurothioglucose (GTG). AF gold exhibited an early phase of decay with high levels of cell-association; whereas, after 72 h cell-associated gold was not detectable. In contrast, GSTM and GTG serum gold values were generally higher than blood values since cell-associated gold rarely occurred. These observations suggest that, in contrast to GSTM and GTG, intravenous administration of AF results in a dynamic equilibrium of gold between the cellular and serum compartments of blood.
Animals↗
Separation and recovery of intact gold-virus complex by agarose electrophoresis and electroelution: application to the purification of cowpea mosaic virus and colloidal gold complex.
Colloidal gold has been coupled to a mutant cowpea mosaic virus (CPMV), which contains 60 cysteine residues on the surface. A purification process was developed to separate the gold-containing viral nanoblocks (VNBs) from the free gold. Agarose electrophoresis was utilized to separate the mixture followed by electroelution of the desired sample to recover the intact virus. Mobility of Au-VNB and free colloidal gold was facilitated by the addition of thioctic acid (TA). 30% of the gold-containing virus was recovered after electroelution as determined by absorbance measurements. Histogram analysis of transmission electron microscopy (TEM) images demonstrated the efficient separation of gold-containing virus from free gold. TEM and scanning electron microscopy (SEM) images indicated that the virus was recovered intact. Monodisperse spherical particles of nominal size of 45 nm were observed under SEM.
Comovirus↗
The silver anniversary of gold: 25 years of the colloidal gold marker system for immunocytochemistry and histochemistry.
Since 1971, when W.P. Faulk and G.M. Taylor published "An immunocolloid method for the electron microscope", colloidal gold has become a very widely used marker in microscopy. It has been used to detect a huge range of cellular and extracellular constituents by in situ hybridization, immunogold, lectin-gold, and enzyme-gold labeling. Besides its use in light microscopic immunogold and lectin-gold silver staining, colloidal gold remains the label of choice for transmission electron microscopy studying thin sections, freeze-etch, and surface replicas, as well as for scanning electron microscopy. The year 1996 is the 25th anniversary of the introduction of colloidal gold as a marker in immunoelectron microscopy and this overview outlines some of the major milestones in the development of the colloidal gold marker system.
Animals↗
Gold(I) efflux from auranofin-treated red blood cells. Evidence for a glutathione-gold-albumin metabolite.
The efflux of gold from red blood cells (RBCs) exposed to 10-100 microM auranofin [the second generation chrysotherapy agent, triethylphosphine-(2,3,4,6-tetra-O-acetyl-1-beta-D-glucopyranosato -S-)gold(I)] was studied. RBCs in whole blood were allowed to accumulate gold, and then were placed in fresh plasma or buffered saline solution. In plasma, the kinetics of efflux were first order in gold with an apparent rate constant of 0.81 +/- 0.18 hr-1. Serum albumin, in plasma or added to a buffered solution, shifted the equilibrium between intra- and extracellular gold in favor of the latter (compared to saline solution). [14C]Glutathione, generated by in situ labeling, also effluxed and associated with the albumin and gold, providing the first direct evidence that the albumin-gold-glutathione complex (AlbSAuSG) may be a circulating metabolite of auranofin formed after both of the original ligands of auranofin are displaced.
Albumins↗
Recovery of gold from gold slag by wood shaving fly ash.
Wood shaving fly ash was used as an alternative adsorbent for gold preconcentration from gold slag. The maximum gold adsorption capacity of wood shaving fly ash washed with tap water (WSFW) at 20, 30, 40, and 60 degrees C was 8.68, 7.79, 7.44, and 7.25 mg(Au)/g(adsorbent), respectively, while of activated carbon it was 76.78, 60.95, 56.13, and 51.90 mg(Au)/g(adsorbent), respectively. Deionized water at 100 degrees C could elute gold adsorbed onto WSFW to 71%. The effect of the increasing temperature of water, 30, 60, and 100 degrees C, implied that the adsorption mechanism was mainly physical adsorption. The negative values of enthalpy change (DeltaH) and free energy change (DeltaG) indicated an exothermic and spontaneous process, respectively. The positive values of entropy change (DeltaS) indicated increasing disorder of the system. The advantages of wood shaving fly ash are the purification of gold and the easier recycling of gold from the gold-adsorbed adsorbent.
Adsorption↗
Impedance sensing of DNA binding drugs using gold substrates modified with gold nanoparticles.
Interfacial interactions between immobilized DNA probes and DNA-specific sequence binding drugs were investigated using impedance spectroscopy toward the development of a novel biosensing scheme. The impedance measurements are based on the charge-transfer kinetics of the [Fe(CN)6]3-/4- redox couple. Compared to bare gold surfaces, the immobilization of DNA and then the DNA-drug interaction on electrode surfaces altered the capacitance and the interfacial electron resistance and thus diminished the charge-transfer kinetics by reducing the active area of the electrode or by preventing the redox species from approaching the electrode. Electrochemical deposition of gold nanoparticles on a gold electrode surface showed significant improvement in sensitivity. DNA-capped gold nanoparticles on electrodes act as selective sensing interfaces with tunable sensitivity due to higher amounts of DNA probes and the concentric orientation of the DNA self-assembled monolayer. The specificity of the interactions of two classical minor groove binders, mythramycin, a G-C specific-DNA binding anticancer drug, netropsin, an A-T specific-DNA binding drug and an intercalator, nogalamycin on AT-rich DNA-modified substrate and GC-rich DNA-modified substrate are compared. Using gold nanoparticle-deposited substrates, impedance spectroscopy resulted in a 20-40-fold increase in the detection limit. Arrays of deposited gold nanoparticles on gold electrodes offered a convenient tool to subtly control probe immobilization to ensure suitably adsorbed DNA orientation and accessibility of other binding molecules.
DNA↗