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PubMedDate not supplied

Clinical pharmacokinetics of oral and injectable gold compounds.

The pharmacokinetics of oral gold (auranofin) in some respects resemble, and in other respects differ from, those of existing parenteral gold compounds such as gold sodium thiomalate (GST). This may in part relate to physicochemical differences as GST is a water-soluble polymeric compound in vitro whereas auranofin is lipid-soluble and characteristically monomeric. Furthermore, intramuscularly administered gold is greater than 95% bioavailable, whereas only 20 to 30% of an orally administered dose of auranofin is absorbed. Following a standard 50mg intramuscular injection of GST, serum gold concentrations rise sharply, peaking between 4 and 8 mg/L in approximately 2 hours and declining to an average of 3 mg/L by 7 days. With repeated injections of GST stable serum concentrations of gold (3 to 5 mg/L) are eventually achieved (usually within 5 to 8 weeks) although absolute concentrations may vary widely between patients. On the other hand, long term treatment with auranofin is associated with lower and more stable serum concentrations of gold (0.5 to 0.7 mg/L), on the standard dosing regimen of 6 mg daily. Both compounds are retained within the body for prolonged periods. However, the amount of gold retained with auranofin is significantly less compared with GST (less than 5% of a tracer dose of auranofin--about 20% of the absorbed dose--is retained by 100 days whereas the retention for a single labelled dose of GST over a similar interval is greater than 50%). Excretory patterns of GST and auranofin also differ. Most of an absorbed dose of GST (greater than 70%) is excreted by the kidneys whereas only 50% of an absorbed (15% of an administered) dose of auranofin is excreted in the urine. Both compounds are avidly bound by plasma proteins and auranofin shows a particularly strong association with circulating cellular elements. In human subjects, parenterally administered gold is widely distributed among bodily tissues, showing a predilection for tissues of the reticuloendothelial system as well as the kidney and adrenal cortex. Comparable studies in humans are not available for auranofin but animal studies have shown comparatively less affinity for the liver, kidney and spleen. Valuable insight has been gained in analysing the comparative pharmacokinetics of oral and injectable gold compounds. Unfortunately, attempts to correlate pharmacokinetic findings with clinical response or pharmacodynamic changes, as a whole, remain largely unsuccessful with these agents.

Administration, Oral↗
PubMed2001

Gold allergy in North America.

OBJECTIVE: To determine the prevalence of allergic reactions to gold among patients tested by the North American Contact Dermatitis Group (NACDG) from 1996 to 1998. METHODS: This is a prospective analysis of patch test results from the 12 centers that comprise the NACDG. Gold was tested as gold sodium thiosulfate (0.5% in petrolatum [pet]), along with 49 other screening allergens, in patients presenting with possible contact dermatitis. RESULTS: Of 4,101 patients tested, 388 (9.5%) had a positive patch test result to gold. Women accounted for 62.8% of the subjects tested and 90.2% of patients positive to gold (P < .0001). The most common sites of dermatitis in gold-allergic patients were the hands (29.6%), face (19.3%), and eyelids (7.5%). Nickel and cobalt allergies, respectively, also were present in 33.5% and 18.3% of gold allergic individuals, as compared with 14.2% and 9.0% of the total population. Gold was the only positive reaction in 15.2% of the 388 patients. CONCLUSION: Gold is a more common allergen than previously reported and might cause facial and eyelid dermatitis. Hypersensitivity to gold is statistically linked to female gender and to allergic reactions to nickel and cobalt.

Allergens↗
PubMed1990

High-resolution localization of hyaluronic acid in the golden hamster oocyte-cumulus complex by use of a hyaluronidase-gold complex.

The distribution of hyaluronic acid in the oocyte-cumulus complexes collected from the oviduct ampulla of superovulated hamsters was revealed by use of hyaluronidase coupled to colloidal gold. On thin sections of Lowicryl-embedded oocyte-cumulus complexes, gold particles were associated specifically with interconnecting fibrillar materials that make up the cumulus matrix. Inside the cumulus cells, gold particles were found over the cisternal membrane of the rough endoplasmic reticulum, in the contents of lysosomes and multivesicular bodies, and over Golgi vesicles of some cumulus cells. A high concentration of gold labeling was observed over the peripheral condensed chromatin and perinucleolar components in the nucleus. The cell surface of the cumulus cells also appeared to be labeled. Gold particles, however, were absent over the mitochondria and lipid vacuoles. In the oocytes, labeling was found to be associated mainly with rough endoplasmic reticulum and arrays of lamellar structures; cortical granules, mitochondria, and coated vesicles were essentially devoid of gold particles. Gold particles were also seen along the plasma membrane of the oocytes and within the perivitelline space. The zona pellucida was not labeled by hyaluronidase-gold. Different control experiments confirmed the specificity of the labeling. Digestion of thin sections with hyaluronidase prior to incubation with hyaluronidase-gold abolished the initial reaction, whereas treatment of thin sections with chondroitinase did not prevent labeling of oocyte-cumulus complexes by hyaluronidase-gold. Although the function of hyaluronic acid in the oocyte-cumulus complex at the time of ovulation and fertilization is not known, the high concentration of this particular compound in the cumulus matrix and the cumulus cells and its specific locations in the perivitelline space and in the superovulated oocytes implicate the significance of its presence and warrant future investigations.

Animals↗
PubMed1995

Quantification of particle sizes with metal replication under standard freeze-etching conditions: a gold ball standard for calibrating shadow widths was used to measure freeze-etched globular proteins.

The real size of platinum-carbon (Pt-C) replicated particles is not directly equivalent to either its metal-coated diameter or its shadow width. This paper describes two indirect methods, shadow widths and coated particle diameters, for determining a particle's actual size beneath a Pt-C replication film. Both produce equivalent measurements using the same standardized conditions: 2.3 nm Pt-C films deposited at a 45 degree angle on an approximately -100 degrees C surface in a 10(-6) torr vacuum. For the first method, gold balls nucleated in a partial pressure of helium and deposited on flat indirect carbon films (root mean square roughness of 0.8 nm) on 400 mesh grids were used as test particles for calibrating shadow widths as a function of particle size. The gold ball test specimens were replicated, and a distribution of Pt-C shadow widths orthogonal to the Pt-C deposition direction was measured and averaged for gold balls 1.5 +/- 0.25 nm, 2.0 +/- 0.25 nm, etc. The diameter of each gold ball was measured within the Pt-C film along with its shadow width because the Pt-C did not obscure or adhere well to the gold. The shadow width distributions for each gold size do not differ significantly from log normal. Two proteins, the lactose repressor and the mitochondrial ATPase, F1, were also used as replication test objects. Negative staining of both proteins was conducted to measure their average diameters. In the second method, a distribution of Pt-C-coated lac repressor diameters perpendicular to the shadow direction was measured. The Pt-C film thickness measured on the quartz crystal monitor was subtracted from the average metal-coated protein diameter to obtain the lac repressor's diameter. The Pt-C-coated particle diameter distributions also did not differ significantly from log normal. While doing this work it was discovered that outgassing the Pt-C electron gun greatly affected Pt-C film granularity: 19 sec produced a high contrast, granular Pt-C film, whereas 120 sec yielded a low contrast, less granular Pt-C film. Both gold balls and protein particles were subjected in separate experiments to either 19 or 120 sec of outgassing of the Pt-C gun prior to Pt-C replication. Outgassing had a profound effect on the average size of the Pt-C shadow widths on both gold and protein particles. The Pt-C gun outgassing procedure also determined the smallest replicated particle that could be resolved. The frequency of some smaller gold ball sizes detected after replication was reduced disproportionately with 19 sec vs. 120 sec outgassing. However, Pt-C gun outgassing did not affect the average measured diameter of the Pt-C-coated protein particles. The "geometric assumption" that each metal-coated particle creates a shadow width the same size as the metal-coated particle diameter was tested using a globular protein. Pt-C replication of protein particles at a 45 degree and 20 degree angle could not confirm the geometric assumption because an average shadow width was always significantly larger than its average Pt-C-coated particle diameter. A model for how the large shadow widths are formed is presented. Gold balls were also replicated at a 45 degree angle with current high resolution conditions at a substrate temperature of -185 degrees C, and the results of these replicas were compared to the results reported here at approximately -100 degrees C.

Calibration↗
PubMed1989

The natural course of gold and penicillamine nephropathy: a longterm study of 54 patients.

To elucidate the natural course of gold and penicillamine nephropathy and to facilitate appropriate clinical management 54 patients with rheumatoid arthritis who developed proteinuria during treatment with intramuscular gold thiomalate (21) or oral D penicillamine (33) were studied in detail throughout the whole of their renal illnesses. Renal biopsy was performed and creatinine clearance and proteinuria were measured serially for a median period of 60 months (range 16-130 months) in the gold treated and 74 months (range 13-158 months) in the penicillamine treated patients. During gold (penicillamine) treatment 48% (43%), 71% (82%) and 86% (91%) of patients had presented with proteinuria by 6, 12 and 24 months of treatment. After stopping gold (penicillamine) treatment proteinuria reached a median maximum of 2.1 g/day (4.2 g/day) at 2 months (1 month) before resolving spontaneously so that by 6, 12 and 18 months 38% (36%), 62% (64%) and 76% (88%) of patients were free of proteinuria. The median initial and most recent creatinine clearances of the gold (penicillamine) treated patients were 77 ml/min (80 ml/min) and 59 ml/min (78 ml/min) respectively and no patients died from or needed treatment for chronic renal failure. HLA B8 and/or DR3 alloantigens were identified in 64% of the gold treated and 56% of the penicillamine treated patients. In the gold (penicillamine) treated patients renal biopsy revealed membranous glomerulonephritis (GN) in 72% (88%), an immune complex mesangial glomerulonephritis in 10% (6%), minimal change nephropathy in 10% (6%) and no significant glomerular abnormalities in 8% (0%). The study has demonstrated the close similarity between gold and penicillamine nephropathy. It has also demonstrated that some 75% of cases develop during the first year of treatment, the proteinuria resolves completely when treatment is withdrawn, progressive deterioration of renal function is most uncommon, corticosteroid therapy is unnecessary and several different types of glomerulonephritis are associated with gold and penicillamine treatment.

Adult↗
PubMed2006

Investigation on the interaction between colloidal gold and human complement factor 4 at different pH by spectral methods.

The interaction between colloidal gold and human complement factor 4 (human C4) at different pH was investigated by spectral methods, including absorption and resonance light-scattering spectrometry. According to the changes of color and absorption spectra of colloidal gold solution in presence of human C4, the interaction between colloidal gold and human C4 was quantitatively investigated using a semi-empirical "flocculation parameter". At the same time, the changes of resonance light-scattering spectra and transmission electron microscopy (TEM) images indicate that the aggregation of colloidal gold happens by electrostatic interaction in presence of human C4 in the pH range 5-6. However, the colloidal gold solution remains stable at pH >6 and pH <5 due to the repulsive electrostatic interaction between colloidal gold and human C4. The flocculation parameter is directly proportional to the concentration of human C4 in the range from 9.7 to 233.0 microgl(-1). In addition, the interactions between the colloidal gold and bovine serum albumin (BSA) as well as human serum albumin (HSA) were also investigated using the same methods. It was found that there was no aggregation of colloidal gold in presence of BSA and HSA in the pH range 5-6. However, when the pH of solution is 4, the aggregation of colloidal gold happens. Because BSA and HSA have different structure, the intensity of aggregation of colloidal gold in presence of BSA is greater than that in presence of HSA at pH 4.

Animals↗
PubMed1997

Lichenoid dermatitis after consumption of gold-containing liquor.

Medicinal gold has a well-known side effect profile that includes mucocutaneous eruptions. We describe three patients with a pruritic dermatitis that began after consumption of a gold-containing alcoholic beverage. Blood and urine gold levels, chemistry panels, hepatitis screens, skin biopsies, and patch tests were performed. The gold-containing liquor was analyzed for the presence and quantity of gold. The liquor consumed by all of the patients was a cinnamon schnapps with free-floating gold-colored flakes. Gold is present in the liquid portion of this liquor and in the solid flakes. Elevated levels of gold in the urine and blood were present in one patient 3 months after last drinking this beverage. Another patient had a positive patch test to gold sodium thiosulfate. All patients experienced improvement of their dermatitis after they stopped drinking the gold-containing liquor.

Adult↗
PubMed2001

Use of gold nanoparticles to enhance capillary electrophoresis.

We describe here the use of gold nanoparticles to manipulate the selectivity between solutes in capillary electrophoresis. Two different gold-based nanoparticles were added to the run buffer. In one case, the nanoparticles were stabilized with citrate ions, but in another study, the gold nanoparticles were capped with mercaptopropionate ions (thiol-stablized). Citrate-stabilized gold nanoparticles were used in conjunction with capillaries treated with poly(diallyldimethylammonium chloride) (PDADMAC). The positively charged PDADMAC layer on the capillary walls adsorbs the negatively charged gold nanoparticles. The model solutes that were used to study the effect of the presence of the citrate-stabilized gold nanoparticles are structural isomers of aromatic acids and bases. The presence of the PDADMAC layer and the PDADMAC plus the gold nanoparticles changes both the electroosmotic mobility and the observed mobility of the solutes. These changes in the mobilities influence the observed selectivities and the separations of the system. Thiol-stabilized gold nanoparticles were used without PDADMAC in the capillary. The model solutes studied in this part are various aromatic amines. In this case as well, the presence of the gold nanoparticles modifies the electroosmotic mobility and the observed mobility of the solutes. These changes in the mobilities are manifested in selectivity alterations. The largest change in the selectivities occurs at low concentrations of the gold nanoparticles in the run buffer. The presence of nanoparticles improves the precision of the analysis and increases the separation efficiency.

Amines↗
PubMed2005

Double hydrophilic block copolymer monolayer protected hybrid gold nanoparticles and their shell cross-linking.

This paper describes the syntheses of core/shell gold nanoparticles stabilized with a monolayer of double hydrophilic block copolymer and their stimuli responsiveness before and after shell cross-linking. The hybrid nanoparticles consist of gold core, cross-linkable poly(2-(dimethylamino)ethyl methacrylate) (PDMA) inner shell, and poly(ethylene oxide) (PEO) corona. First, diblock copolymer PEO-b-PDMA was prepared via the reversible addition-fragmentation chain transfer (RAFT) technique using a PEO-based macroRAFT agent. The dithioester end group of PEO-b-PDMA diblock copolymer was reduced to a thiol end group. The obtained PEO-b-PDMA-SH was then used to prepare diblock copolymer stabilized gold nanoparticles by the "grafting-to" approach. 1,2-Bis(2-iodoethoxy)ethane (BIEE) was utilized to selectively cross-link the PDMA residues in the inner shell. The stimuli responsiveness and colloidal stability of core/shell gold nanoparticles before and after shell cross-linking were characterized by laser light scattering (LLS), UV-vis transmittance, and transmission electron microscopy (TEM). At pH 9, the average hydrodynamic radius Rh of non-cross-linked hybrid gold nanoparticles starts to increase above 35 degrees C due to the lower critical solution temperature (LCST) phase behavior of the PDMA blocks in the inner shell. In contrast, Rh of the shell cross-linked gold nanoparticles were essentially independent of temperature. Core/shell gold nanoparticles before and after shell cross-linking exhibit reversible swelling on varying the solution pH. Compared to non-cross-linked core/shell gold nanoparticles, shell cross-linking of the hybrid gold nanoparticles leads to permanent core/shell nanostructures with much higher colloidal stability and physically isolates the gold core from the external environment.

Gold↗
PubMed2000

Immunosuppressant effect of gold on IgG subclasses and IgE; evidence for sparing of Th2 responses.

We set out to examine the effect of gold treatment on the Th2-dependent antibodies IgG4 and IgE in relation to other IgG subclasses in patients with rheumatoid arthritis (RA). Eighty-five gold-treated RA patients and 82 RA controls were studied. Serum IgG subclass concentrations were measured by ELISA, IgE was measured by automated enzyme immunoassay. Samples were studied serially in 13 gold-treated patients and in 11 patients with gold-induced adverse events. There was a significant reduction in the concentration of IgG1, IgG2 and IgG3 in gold-treated RA patients compared with RA controls (P 0.004-0.019), whereas IgG4 was less significantly reduced in gold-treated patients (P = 0.044) and there was no difference in IgE. In serial samples there was a significant fall in the concentration of IgG1 (P = 0.001), IgG2 (P = 0.001) and IgG3 (P = 0.026) with time but no change in IgG4 and IgE. The development of gold-induced adverse events was not associated with any change in the concentration of each IgG subclass or IgE. Deficiencies of IgG subclasses were found in 30% of gold-treated RA patients and 8.5% of RA controls, and were associated in gold-treated patients with a longer disease duration (P = 0.003) and with erosive disease (P = 0. 03). IgG2 was affected most frequently and in the majority of these cases subnormal specific IgG2 binding to widespread polysaccharide antigens (Pneumovax II) was found. Gold induces an overall immunosuppressant effect on IgG subclasses, with a deficiency in 21. 5%, adjusted for controls. The effect on the Th2-dependent antibodies IgG4 and IgE is less marked, suggesting a sparing of Th2 responses.

Antirheumatic Agents↗
PubMed2002

Gold and its relationship to neurological/glandular conditions.

Despite increasing sales of gold supplements, and claims of benefits for neurological and glandular conditions, gold has received little attention in modern medical literature except as a drug for rheumatoid arthritis. Historically, however, gold had a reputation as a "nervine," a therapy for nervous disorders. A review of the historical literature shows gold in use during the 19th century for conditions including depression, epilepsy, migraine, and glandular problems such as amenorrhea and impotence. The most notable use of gold was in a treatment for alcoholism developed by Keeley (1897). In the modern medical literature, gold-containing medicines for rheumatoid arthritis are known to have occasional neurotoxic adverse effects. There are also a few studies suggesting a role for gold as a naturally occurring trace element in the reproductive glands. One small recent study demonstrated a possible positive effect of gold on cognitive ability. There is a need for more experimental and clinical research of the neuropharmacology and neurochemistry of gold, and for the exploration of gold's possible role as a trace element.

Antirheumatic Agents↗
PubMed1981

alpha 2-macroglobulin adsorbed to colloidal gold: a new probe in the study of receptor-mediated endocytosis.

alpha 2-Macroglobulin (alpha 2 M) was adsorbed to colloidal gold and used as a new tool in the study of receptor-mediated endocytosis. alpha 2 M-gold is easy to prepare and is clearly visualized at the electron microscope level. When cells were incubated with alpha 2 M-gold at 0 degrees C, gold was visualized both diffusely over the cell surface and concentrated in coated pits. After cells to which alpha 2 M-gold had been bound at 0 degrees C were warmed, the gold was rapidly internalized into uncoated vesicles, previously termed receptosomes. After 30 min of incubation or longer, gold was found in small lysosomes and, later, in large lysosomes and very small vesicles in the region of the Golgi complex. This pattern of localization is similar to that previously described, using peroxidase-labeled anti-alpha 2 M antibodies. By incubating cells with both alpha 2 M-gold and vesicular stomatitis virus (VSV), we studied the internalization of these two markers simultaneously. VSV and alpha 2 M-gold rapidly clustered in the same coated pits and were internalized in the same receptosomes. Proteins and hormones adsorbed to gold may be useful in the study of receptor-mediated endocytosis.

Animals↗
PubMedDate not supplied

Changes in corneal topography with upper eyelid gold weight implants.

PURPOSE: To determine the effect of upper eyelid gold weight implantation on corneal astigmatism. METHODS: This is a prospective, cohort study. Eighteen eyes of 18 patients underwent upper eyelid gold weight implantation for facial nerve palsy. Nine of these patients recovered facial nerve function and underwent elective removal of the gold weight. Corneal topography was performed before and after gold weight implantation. Corneal topography was also performed after gold weight removal in patients who recovered from facial nerve paralysis. RESULTS: With-the-rule corneal astigmatism increased significantly by 1.4 diopters (D) +/-2.0, from a mean of 0.3 to 1.7 D after gold weight implantation (p = 0.034). With-the-rule corneal astigmatism in patients who had gold weight removal decreased by 1.2 +/- 2.1 D, from 2.2 to 1.0 D after gold weight removal (p = 0.136). CONCLUSIONS: Upper eyelid gold weight implantation causes an increase in corneal astigmatism, predominantly in the vertical axis, which appears to be reversible on removal of the gold weight.

Adult↗
PubMed1984

Triethylphosphine gold: cellular uptake and disposition after single and repeated oral doses in rats.

The tissue and subcellular pharmacokinetics of gold following single and repeated oral doses of triethylphosphine gold (auranofin) has been studied in rats. After a single dose, the tissue and subcellular gold levels were 5-10 times lower than those reached with injectable gold compounds. In the liver tissues, gold concentrations peaked within 24 h followed by a biphasic clearance, with an initial rapid phase (t1/2 32 h) and a slow terminal phase (t 1/2 11 days). Renal gold concentrations continued to increase for 3 to 5 days and then decreased exponentially with a first order t 1/2 of about 7 days. Intracellularly, between 60-80% of hepatic and 50-70% of renal gold was present in the cytosol. In rats given repeated doses of auranofin, the hepatic and renal gold concentrations were 3-5 times higher than those measured after a single dose. The proportion of cellular gold present in the cytosol was markedly lower, with 43% in the liver and 30% in kidney tissues. In both the liver and kidney, gold concentrations were dose-dependent, whereas in the gastrointestinal tissues the increases as a function of dose were minimal.

Administration, Oral↗
PubMed1976

Selective concentration and localization of gold in macrophages of synovial and other tissues during and after chrysotherapy in rheumatoid patients.

Gold distribution was studied in the tissues of 7 rheumatoid patients who had died from 0 to 23 years after stopping chrysotherapy (sodium aurothiomalate) and in 23 samples of synovial tissue removed surgically at intervals during chrysotherapy in 5 patients. After the application of a highly specific staining technique, the cellular localization of gold was examined microscopically in various tissues: the amounts of gold in selected areas of the same specimens which had been examined microscopically were then measured by neutron activation analysis. During active chrysotherapy gold was abundant in synovial lining cells except where a fibrin layer was present on the surface; after stopping chrysotherapy, gold disappeared from the synovial lining cells. Gold accumulated progressively in the subsynovial connective tissues during chrysotherapy, but was not uniformly distributed, and bore no relationship to fluctuations in serum gold levels. Gold deposition was not confined to joint tissue, but was found within the macrophages of many organs, renal tubular epithelium, and, after recent chrysotherapy, in seminiferous tubules, hepatocytes, and adrenal cortical cells. Gold persisted in synovial and other tissues for up to 23 years after chrysotherapy was stopped. The overall findings indicated that gold is selectively concentrated within inflamed synovial tissues during chrysotherapy.

Aged↗
PubMed1991

Carcinoma of the lung in Ontario gold miners: possible aetiological factors.

A cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.

Adenocarcinoma↗
PubMed2001

Gold-coated NIR stents in porcine coronary arteries.

BACKGROUND: As endovascular stents are altered to add functionality, eg, by adding radiopaque coatings, biocompatibility may suffer. METHODS AND RESULTS: We examined the vascular response in porcine coronary arteries to stainless steel gold-coated NIR stents (7-cell, Medinol, Inc). Stents, 9 and 16 mm in length, were left bare or coated with a 7-microm layer of gold. Physical and material effects were examined in four different gold-coated stent types, two at each length that either had the coating applied to the standard strut, ie, gold coated thicker than controls, or had the coating applied to thinned struts, ie, gold coated of the same thickness as control struts. Simple gold coating exacerbated intimal hyperplastic and inflammatory reactions over 28 days, but postplating thermal processing smoothed the coating surface and negated the adverse tissue response to gold. The relative amounts of base steel and gold coating and their resistances to expansion and collapse determined the extent of stent recoil. CONCLUSIONS: Gold coatings enhance the radiopacity of steel stents, but not without effects on vascular repair. Material effects predominate and can be abrogated by heating coated stents to alter surface finish and material purity. Clinical results may suffer unless consideration is given to material and physical effects of gold.

Animals↗
PubMed1986

[Nephrotoxic effect of gold sodium thiomalate in rats--ultrastructual observations using electronmicroscopy and X-ray energy dispersive analysis].

The purpose of this study is to demonstrate renal injuries by gold sodium thiomalate (G) with ultrastructual changes and gold deposition in kidney tissue using X-ray energy dispersive analysis (XEDA). Twenty-five mg of G containing 12.1 mg of Au was injected into rats intraperitoneally. The rats were divided into 5 groups. Group 1 was sacrificed 6 hours after the injection of G, and group 2 after 24 hours, group 3 after 72 hours and group 4 after 144 hours. Group 5 consisted of the control-rats which were provided with injections of saline. Gold contents in kidneys, liver, lungs and spleen were measured using the flameless atomic absorption method. XEDA was also performed in order to confirm the gold deposition in tissue. Among the organs, only the kidney showed remarkable changes with increased weight. Group 1 already showed marked azotemia which reached to the maximum level in group 3. The amount of gold content in the organs did not change significantly in spite of a marked reduction of serum gold concentration among the 4 groups. Histological examinations revealed marked degeneration and necrosis of pars recta in proximal tubules, although no prominent abnormalities of glomeruli could be observed. Using an electron microscope, many electron dense particles in lysosome were noticed, mainly in proximal tubules. We also found these particles in lysosome of glomerular epithelial cells. Using XEDA, these electron dense particles were demonstrated to be gold, since characteristic energy of gold was found. In conclusion, the kidney was shown to be the most accumulative organ of gold. G caused acute extensive necrosis of proximal tubules. Gold was demonstrated as electron dense particles in lysosomes mainly in proximal tubules, but also partly in glomeruli. Therefore, it was confirmed that a large amount of G had a strong nephrotoxic effect in rats.

Animals↗