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PubMed1994

Randomized trial of switching rheumatoid arthritis patients in remission with injectable gold to auranofin.

This prospective unblinded 24-month-study compared the therapeutic value of oral gold with injectable gold to maintain rheumatoid arthritis (RA) patients in clinical remission and prevent the progression of erosive disease. Forty-six patients with definite RA in remission with injectable gold were randomized into two groups: a control group, continued on maintenance injectable gold (Solganal, aurothioglucose, 50-100 mg, intramuscularly, 2 to 4 weeks); and an experimental group, switched to oral gold (6-9 mg auranofin by mouth daily). Only 29% of the original 24 oral gold patients remained on assigned treatment at 24 months compared with 64% of the injectable gold group. By six months, over one-half of the oral gold patients had electively stopped their randomized therapy. Sixty-seven percent of the oral gold patients had adverse reactions, mostly gastrointestinal complaints, compared with one proteinuria in the injectable gold group. The oral gold group experienced significantly more deterioration in all the primary measures of treatment effect over the follow-up period. At the termination of the trial, 88% of the group had increases of 5 or more points in radiographic scores suggesting progression of erosive disease compared with only 29% of the control group. These data suggest that oral gold is not an effective substitute for injectable gold in maintaining remission in rheumatoid arthritis.

Administration, Oral↗
PubMed2005

Restenosis in gold-coated renal artery stents.

BACKGROUND: Gold coating improves stent visibility under fluoroscopy. This is particularly valuable for precise stent placement during renal artery stenting (RAS). There is conflicting evidence regarding restenosis with gold-coated stents. To evaluate the effect of gold coating on restenosis after renal stenting, we reviewed the results of all patients undergoing RAS in our practice. METHODS: A retrospective cohort study of all patients undergoing RAS between June 2000 and September 2003 was performed. During this time, both gold-coated and stainless steel stents were used. Restenosis (>60% diameter) was determined by serial follow-up duplex exams (peak systolic velocity >180 cm/s and renal-aortic ratio >3.5). Restenosis rates were determined by using the Kaplan-Meier life-table method. Variables potentially affecting restenosis were evaluated with the log-rank test and Cox proportional hazards modeling. RESULTS: RAS was performed in 97 arteries (78 patients). Gold-coated (NIRoyal) stents were placed in 59 arteries (48 patients). Stainless steel stents (Corinthian, Genesis, and Herculink) were placed in 38 arteries (34 patients). Patient demographics, indication for treatment, technical success, and complications did not differ between gold and stainless steel stent groups. Mean follow-up was 15 months for gold-coated stents and 18 months for stainless steel stents (NS). By life-table method, 1-year and 2-year freedom from restenosis rates were 84% and 78% in arteries treated with stainless steel stents versus 69% and 39% in those treated with gold-coated stents (P = .012, log-rank test). By multivariate analysis, only the use of gold-coated stents (P = .018; hazard ratio [HR], 3.3; 95% confidence interval [CI], 1.2 to 8.7) and bilateral disease (P = .046; HR, 2.3; 95% CI, 1.02 to 5.2) predicted restenosis. Stent diameter, patient demographics, and indication for RAS had no effect on restenosis by univariate analysis. According to American Heart Association criteria, 87% of patients in the stainless steel group had improved blood pressure at 1 year, compared with 77% in the gold-coated stent group (Kaplan-Meier; P = .042, log-rank test). There were no significant differences in the effect of RAS on serum creatinine levels between the two groups. CONCLUSION: Gold-coated renal stents had a substantially higher rate of restenosis than stainless steel stents in our series. These findings have led us to abandon the use of gold-coated stents for RAS. Patients who have received gold-coated stents for the treatment of atherosclerotic renal artery stenosis should be followed closely for evidence of restenosis.

Aged↗
PubMed2005

Photoinduced electron transfer between chlorophyll a and gold nanoparticles.

Excited-state interactions between chlorophyll a (Chla) and gold nanoparticles have been studied. The emission intensity of Chla is quenched by gold nanoparticles. The dominant process for this quenching has been attributed to the process of photoinduced electron transfer from excited Chla to gold nanoparticles, although because of a small overlap between fluorescence of Chla and absorption of gold nanoparticles, the energy-transfer process cannot be ruled out. Photoinduced electron-transfer mechanism is supported by the electrochemical modulation of fluorescence of Chla. In absence of an applied bias, Chla cast on gold film, as a result of electron transfer, exhibits a very weak fluorescence. However, upon negatively charging the gold nanocore by external bias, an increase in fluorescence intensity is observed. The negatively charged gold nanoparticles create a barrier and suppress the electron-transfer process from excited Chla to gold nanoparticles, resulting in an increase in radiative process. Nanosecond laser flash experiments of Chla in the presence of gold nanoparticles and fullerene (C60) have demonstrated that Au nanoparticles, besides accepting electrons, can also mediate or shuttle electrons to another acceptor. Taking advantage of these properties of gold nanoparticles, a photoelectrochemical cell based on Chla and gold nanoparticles is constructed. A superior performance of this cell compared to that without the gold film is due to the beneficial role of gold nanoparticles in accepting and shuttling the photogenerated electrons in Chla to the collecting electrode, leading to an enhancement in charge separation efficiency.

Chlorophyll↗
PubMed2005

Biotin-streptavidin-induced aggregation of gold nanorods: tuning rod-rod orientation.

We report herein biotin-streptavidin-mediated aggregation studies of long gold nanorods. We have previously demonstrated end-to-end linkages of gold nanorods driven by the biotin-streptavidin interaction (Caswell et al. J. Am. Chem. Soc. 2003, 125, 13914). In that report, the specific binding of biotin disulfide to the gold nanorod edges was achieved due to the preferred binding of thiol molecules to the Au[111] surface (gold nanorod ends) as opposed to the gold nanorod side faces. This led to the end-end linkage of gold nanorods upon subsequent addition of streptavidin. In this report we demonstrate a simple procedure to biotinylate the entire gold nanorod surface and subsequently form a 3-D assembly by addition of streptavidin. Gold nanorods were synthesized by the three-step seeding protocol documented in our previous articles. The surface of gold nanorods was further modified by a layer of a weak polyelectrolyte, poly(acrylic acid), PAA. A biotin molecule which has an amine group at one end (biotin-PEO-amine) was anchored to the carboxylic acid group of the polyelectrolyte using the well-known carbodiimide chemistry. This process biotinylates the entire gold nanorod surface. Addition of streptavidin further leads to aggregation of gold nanorods. A closer look at the aggregates reveals a preferential side-to-side assembly of gold nanorods. The gold nanorods were characterized at each stage by UV-vis spectroscopy, light scattering, and transmission electron microscopy (TEM) measurements.

Biotin↗
PubMed1993

Long-lasting allergic patch test reaction caused by gold.

Allergic contact dermatitis caused by gold is rare, and only isolated cases have been reported. Patch testing with gold may cause a long-lasting reaction. The purpose of this study is to describe a well-studied case of gold allergy caused by dental gold crowns. A gold-sensitized patient and a non-sensitized control subject were examined using patch tests, immunohistochemistry, electron microscopy and blast transformation reactions. Sodium thiosulfate, auranofin and sodium thiomalate gave positive patch test reactions. Immunohistochemistry and electron microscopy were performed from biopsies taken from allergic patch test reactions caused by gold sodium thiosulfate 1 day and 17 days after applying the patches, from normal skin and from a 17-day-old allergic patch test reaction caused by ammonium persulfate. Down-regulation had taken place by 17 days in the allergic ammonium persulfate reaction, but not in the 17-day allergic gold test reaction. The patient reacted to all but one of the gold-induced blast transformation tests, sodium chloroaurate being non-inductive. The non-sensitized control subject did not exhibit any reactions. In conclusion, gold sodium thiosulfate, gold sodium thiomalate and auranofin can be used as patch test substances for gold allergy, though long-lasting allergic patch test reactions may develop. In vitro gold salt induced blast transformation is an alternative test for gold allergy. The slow down-regulation of the allergic patch test reactions needs to be studied further.

Crowns↗
PubMedDate not supplied

Reasons for placement, replacement, and age of gold restorations in selected practices.

A total of 745 gold restorations were surveyed concerning the reasons for their placement and replacement. Cast gold restorations (n = 480) were placed due to primary caries (23%), replacement of amalgam (39%), and composite restorations (9%), or due to failure of existing gold restorations (29%). The main reasons for replacement of cast gold restorations were fracture of tooth (36%) and secondary caries (22%). The main reasons for the placement of compacted gold restorations (n = 265) were treatment of primary caries (40%), failure of an existing compacted gold restoration (26%), removal of another type of restoration (18%), and repair of a defective margin of a casting (16%). The main reasons for replacement of compacted gold restorations were inclusion into larger restorations (29%) and secondary caries (21%). The longevity of failed gold restorations was recorded for 111 restorations. The mean age for failed cast and compacted gold restorations was about 18.5 years (range 5-41 years). The ages of 2564 gold restorations in situ, 1689 castings, and 875 compacted gold restorations were recorded. The median and mean ages for gold castings were about 15 and 16 years and for compacted gold restorations about 17 and 18 years.

Dental Restoration, Permanent↗
PubMed2005

DFT and in situ EXAFS investigation of gold/ceria-zirconia low-temperature water gas shift catalysts: identification of the nature of the active form of gold.

A combined experimental and theoretical investigation of the nature of the active form of gold in oxide-supported gold catalysts for the water gas shift reaction has been performed. In situ extended X-ray absorption fine structure (EXAFS) and X-ray absorption near-edge structure (XANES) experiments have shown that in the fresh catalysts the gold is in the form of highly dispersed gold ions. However, under water gas shift reaction conditions, even at temperatures as low as 100 degrees C, the evidence from EXAFS and XANES is only consistent with rapid, and essentially complete, reduction of the gold to form metallic clusters containing about 50 atoms. The presence of Au-Ce distances in the EXAFS spectra, and the fact that about 15% of the gold atoms can be reoxidized after exposure to air at 150 degrees C, is indicative of a close interaction between a fraction (ca. 15%) of the gold atoms and the oxide support. Density functional theory (DFT) calculations are entirely consistent with this model and suggest that an important aspect of the active and stable form of gold under water gas shift reaction conditions is the location of a partially oxidized gold (Audelta+) species at a cerium cation vacancy in the surface of the oxide support. It is found that even with a low loading gold catalysts (0.2%) the fraction of ionic gold under water gas shift conditions is below the limit of detection by XANES (<5%). It is concluded that under water gas shift reaction conditions the active form of gold comprises small metallic gold clusters in intimate contact with the oxide support.

Journal Article↗
PubMed1983

Comparative safety and efficacy of auranofin and parenteral gold compounds: a review.

The comparative safety and efficacy of the orally active gold compound, auranofin, and parenteral gold compounds, principally gold sodium thiomalate, are reviewed. No difference in efficacy was detected in eight of the 12 published studies which compared auranofin and gold sodium thiomalate. Two studies favoured auranofin and two gold sodium thiomalate. Other parenteral gold compounds appeared more effective than auranofin. Adverse reactions and withdrawal rate from parenteral gold was found to be 2-3 times greater than from auranofin. Withdrawals due to inefficacy were found to be higher for auranofin than for parenteral gold although the incidence of inefficacy in the parenteral gold treated population was lower than that reported in other series. The nature of side effects from the two treatments was noticeably different; lower bowel symptoms with auranofin, and mucocutaneous lesions with parenteral gold compounds. Significant laboratory index changes were uncommon with both treatments, proteinuria being the most usual reason for withdrawal. Again the incidence of proteinuria and other laboratory abnormalities was less in the parenteral gold group than previously reported. Auranofin is possibly as effective and is definitely safer than parenteral gold compounds, and allows for longer periods of treatment.

Anti-Inflammatory Agents↗
PubMed1998

Improvement of bond strength in metal-ceramic systems using a gold intermediate layer.

The mechanism of bonding between metal and ceramic in systems using the functionally graded method with pure gold and gold mixture as a primer was examined. Four types of samples, porcelain, porcelain-gold, porcelain-metal and porcelain-gold-metal were prepared. The gold intermediate layer was fired at 1000 degrees C. For porcelain and metal, low-fusing opaque, body porcelain and palladium alloy were used. The intermediate layer was composed of three layers; pure gold, gold-palladium and gold-porcelain layer. During the bending test of each sample, the porcelain peeled away from the porcelain-metal system, while porcelain with the gold intermediate layer remained on the metal surface even after maximal loading. The bond strength of the porcelain-gold-metal system was much higher than that of the porcelain-metal system, and the toughness of the former was much greater than that of the latter. Laser microscopy and scanning electron microscopy (SEM) showed a smooth interface between the intermediate layer and the metal which suggested proper chemical bonding, and no gap was observed. At the interface between the porcelain and the gold intermediate alloy, a good mechanical anchor lock was observed. Electron probe microanalysis (EPMA) showed a clear distribution of each element (e.g. Si, Au and Pd) in the porcelain, gold intermediate layer and metal frame.

Dental Bonding↗
PubMed2006

Gold(III) compound is a novel chemocytotoxic agent for hepatocellular carcinoma.

Recently, a series of gold(III) meso-tetraarylporphyrins that are stable against demetallation in physiological conditions have been synthesized. In the present study, the antitumor effects of one of these compounds, gold(III) meso-tetraarylporphyrin 1a (gold-1a) was investigated in an orthotopic rat hepatocellular carcinoma (HCC) model as well as using a HCC cell line. The rat HCC model was induced by injection of rat hepatoma cells, McA-RH7777, into the left lobe of the liver. Seven days after tumor cell inoculation, gold-1a was injected directly into the tumor nodule at different doses, followed by the same doses via intraperitoneal injection twice a week. Gold-1a administration significantly prolonged the survival of HCC-bearing rats. Importantly, gold-1a induced necrosis as well as apoptosis in the tumor tissues, but not in the normal liver tissues. Furthermore, gold-1a treatment neither caused significant drop in body weight of the rats nor affected plasma aspartate aminotransferase level. In the in vitro studies, we observed that gold-1a treatment inhibited the proliferation of McA-RH7777 cells. Gold-1a upregulated genes that increase apoptosis, stabilize p53, decrease proliferation and downregulated genes playing roles in angiogenesis, invasion, and metabolism, as demonstrated by microarray. In particular, the compound upregulated 2 members of the growth arrest and DNA damage (Gadd) inducible gene family, Gadd34 and Gadd153. Suppression of Gadd34 and Gadd153 in McA-RH7777 cells by small hairpin RNA reduced the gold-1a-induced apoptosis and growth inhibition, indicating that gold-1a mediated its effects via upregulation of Gadd34 and Gadd153. Results from our study demonstrated that gold-1a might be a novel promising chemocytotoxic agent for treating HCC.

Alanine Transaminase↗
PubMed1980

Action of gold salts in some inflammatory and immunological models.

Several gold salts were compared in kaolin-induced rat paw oedema, u.v. erythema in guinea pigs, delayed type hypersensitivity and humoral immunity in mice, and adjuvant-induced arthritis in the rat. In the latter the additional parameters of serum gold and copper levels and lysosomal enzyme activity were determined. In addition, the in vitro inhibition of several lysosomal enzymes derived from mouse macrophages was studied. The gold compounds examined were aurothiomalate, aurothioglucose, triethylphosphine gold chloride (SK & F 36914) and its glucopyranoside derivative (SK & F D-39162), triphenylphosphine gold chloride and sodium gold chloride dihydrate. SK & F 36914 and SK & F D-39162 has significant activity after oral dosage upon paw kaolin and u.v. erythema in rats and guinea pigs, respectively. Gastric swelling also occurred. In Wistar rats, adjuvant arthritis was little affected by the gold salts but in the Lewis rats there was suppression. In both strains there was less elevation in serum copper levels with treatment by SK & F 36914 and SK & F D-39162, but not by aurothiomalate. None of the compounds had any measurable effect on delayed hypersensitivity or humoral antibody levels in mice. The in vitro activities of cathepsin B1 and cathepsin D were inhibited by all the gold compounds. Reactivity of gold compounds with glutathione and cysteine in vitro was dependent on compound solubility and the nature of the gold ligand. Considerable differences exist between the profiles of activity for the different gold salts evaluated. These observations indicate that some gold salts do possess anti-inflammatory activity with a potency similar to that of indomethacin.

Animals↗
PubMedDate not supplied

Role of metallothionein in cellular uptake and disposition of gold sodium thiomalate.

Rat liver and kidney tissue uptake of gold and its localization in the cytosol was studied following various doses of gold sodium thiomalate (GST). The timecourse of gold incorporation into intracellular gold-binding ligands following repeated injections of GST was also investigated (11 injections, one dose/week). Results show that between 30 and 60% of the hepatic and renal gold was localized in the cytosol over a wide range of GST doses. This was also true following repeated doses. In the kidney, the binding of gold to high molecular weight (HMW) proteins was saturated after the third GST dose, while incorporation into the metallothioneins (MT) continued to increase, accounting for as much as 50% of cytosolic gold. On the other hand the binding to hepatic MT was about 10x lower, and the proportion of cytosolic gold incorporated into the MT, decreased from 30% (after first 3 GST injections) to about 15% (following the last 3 injections). The results show that the stimulation of MT biosynthesis in different tissues as a response to the injected GST is not the same and varies within each organ with the dose and/or the duration of repeated exposure. In the liver, the ability of gold to induce MT synthesis was limited and the importance of MT in the cellular uptake and disposition of gold may largely be confined to the kidneys. It is suggested that besides playing a possible role in the detoxification of cellular gold, particularly in the kidney, MT may also contribute towards the retention and localization of gold in the tissues.

Animals↗
PubMed1983

Auranofin versus injectable gold. Comparison of pharmacokinetic properties.

The new oral gold compound auranofin differs pharmacokinetically from the existing injectable gold compounds such as gold sodium thiomalate. Following a standard 50 mg intramuscular injection of gold sodium thiomalate, plasma gold levels rise sharply, peak between 400 and 800 micrograms/dl in approximately two hours, then decline to approximately 300 micrograms/dl by seven days. With repeated 50 mg weekly injections, stable plasma concentrations are gradually achieved, although absolute levels vary greatly among individual subjects. On the other hand, auranofin is associated with lower (50 to 70 micrograms/dl) and more predictable plasma concentrations. Single-dose kinetic studies using isotopically labelled gold show that the plasma disappearance half-time for gold sodium thiomalate is relatively rapid (approximately six days) compared with 17 days for auranofin. Both compounds are retained within the body over prolonged periods. Retention of auranofin is much less, about 1 percent of the original tracer dose remaining at 180 days, compared with more than 30 percent retention of gold sodium thiomalate. Excretory pathways are notable different. The majority of gold sodium thiomalate (greater than 70 percent) is excreted by the kidneys, with the remaining fraction appearing erratically in the stool. In contrast, the enteric pathway represents the major excretory route for auranofin, with nearly 85 percent of the dose eventually recoverable in the stool and less than 15 percent in the urine. In human subjects, parenterally administered gold is almost universally dispersed among body tissues, although highest concentrations occur in the organs of the reticuloendothelial system and the adrenal and renal cortices. Comparable studies are not available for auranofin, but animal studies show comparatively less affinity for liver, kidney, and spleen. To date, attempts to correlate the pharmacokinetics of the injectable gold compounds with clinical response and toxicity have been largely unsuccessful. The distinctive pharmacokinetic profile of auranofin, when compared with gold sodium thiomalate, may nonetheless account in part for the clinical and pharmacologic differences between these compounds.

Animals↗
PubMed1982

The effect of zinc and copper pretreatment on the binding of gold (I) to hepatic and renal metallothioneins.

In the first part of this study, single s.c. injections of gold (I) sodium thiomalate were given to male Wistar rats at various dose levels and sacrificed either at 48 hr or 4 days later. The results indicate that though metallothioneins play a significant role in the sequestration of renal gold, the ability of gold itself to induce synthesis of the metalloprotein was limited in the kidneys and practically insignificant in the liver. Pre-injection with zinc however, (4 mg/kg body wt), significantly (P less than 0.01) enhanced the uptake of gold into the metallothioneins both, in the liver as well as the kidneys. The pretreatment increased the proportion of cytosolic gold incorporated into the thioneins from 29% to 48% in the kidneys and from 22% to 47% in the liver. Concurrent increases in the uptake of zinc and copper into the thioneins was also observed. Pre-injection with copper induced a similar effect in the kidneys only. There was no significant difference in the overall uptake of gold into the cytosol itself between the control animals (injected with gold only) and those pretreated with either zinc or copper. This indicated that the increased uptake of gold into the thioneins in the pretreated animals were due to enhanced synthesis of metallothioneins and subsequent increased binding of gold to thioneins rather than increased levels of intracellular gold itself. It is suggested that increased protection against the deposition and possible toxicity of gold in the cell organelles of the liver and kidney tissues may be provided by an increased binding of gold to metallothioneins through pretreatment with zinc, and to a lesser extent copper.

Animals↗
PubMed2005

Estimation of tumour dose enhancement due to gold nanoparticles during typical radiation treatments: a preliminary Monte Carlo study.

A recent mice study demonstrated that gold nanoparticles could be safely administered and used to enhance the tumour dose during radiation therapy. The use of gold nanoparticles seems more promising than earlier methods because of the high atomic number of gold and because nanoparticles can more easily penetrate the tumour vasculature. However, to date, possible dose enhancement due to the use of gold nanoparticles has not been well quantified, especially for common radiation treatment situations. Therefore, the current preliminary study estimated this dose enhancement by Monte Carlo calculations for several phantom test cases representing radiation treatments with the following modalities: 140 kVp x-rays, 4 and 6 MV photon beams, and 192Ir gamma rays. The current study considered three levels of gold concentration within the tumour, two of which are based on the aforementioned mice study, and assumed either no gold or a single gold concentration level outside the tumour. The dose enhancement over the tumour volume considered for the 140 kVp x-ray case can be at least a factor of 2 at an achievable gold concentration of 7 mg Au/g tumour assuming no gold outside the tumour. The tumour dose enhancement for the cases involving the 4 and 6 MV photon beams based on the same assumption ranged from about 1% to 7%, depending on the amount of gold within the tumour and photon beam qualities. For the 192Ir cases, the dose enhancement within the tumour region ranged from 5% to 31%, depending on radial distance and gold concentration level within the tumour. For the 7 mg Au/g tumour cases, the loading of gold into surrounding normal tissue at 2 mg Au/g resulted in an increase in the normal tissue dose, up to 30%, negligible, and about 2% for the 140 kVp x-rays, 6 MV photon beam, and 192Ir gamma rays, respectively, while the magnitude of dose enhancement within the tumour was essentially unchanged.

Animals↗
PubMed1985

Intracellular transport of transferrin- and asialoorosomucoid-colloidal gold conjugates to lysosomes after receptor-mediated endocytosis.

Proteins coupled to colloidal gold particles have been widely used to visualize the uptake and intracellular transport of specific ligands by receptor-mediated endocytosis. The intracellular route of lysosome-directed ligands such as asialoglycoproteins (ASGP) are apparently unaltered by conjugation to gold, but the pathway of transferrin, a ligand that normally recycles to the cell surface, was reported to be altered by conjugation to 15-20 nm gold. In this study, we sought to determine whether a smaller transferrin-gold probe would recycle, and whether it might enter the same endosomal and lysosomal compartments as does a larger, lysosome-directed ASGP gold probe by visualizing their simultaneous uptake in human hepatoma (HepG2) cells. In the same cells, endocytosis of fluid-phase protein was followed using the soluble tracer native ferritin; lysosomal compartments were identified by acid phosphatase cytochemistry; and cell surfaces were labeled with ruthenium red or cationized ferritin. During the first 10 min of uptake at 37 degrees C, specific receptor-bound ferrotransferrin (FeTf)-8 nm gold and asialoorosomucoid (ASOR)-20 nm gold were clustered together in coated pits and entered the same coated vesicles, smooth vesicles, and tubules in the peripheral cytoplasm. At later times, however, transferrin-gold did not return to the cell surface; unlike native transferrin, this gold probe accompanied ASOR-gold into multivesicular bodies (MVB). The MVBs that contained probes were at first devoid of acid phosphatase activity, but at 30 min, enzyme activity was detected in a few MVBs. Native ferritin was present, along with gold probes, in all compartments of the endocytic pathway. We conclude that the normal intracellular pathway of transferrin is altered by its association with a colloidal gold particle.

Asialoglycoproteins↗
PubMed1993

Immunogold labeling of calcium ATPase in sarcoplasmic reticulum of skeletal muscle: use of 1-nm, 5-nm, and 10-nm gold.

We evaluated the use of immunogold electron microscopy to study the distribution of calcium ATPase in the sarcoplasmic reticulum membrane of skeletal muscle. We examined (a) 1-nm gold labeling, (b) the effect of gold size on immunolabeling, and (c) the densities of gold particles in areas of maximal labeling in fibers from rat extensor digitorum longus and pig gracilis muscles. The technique allowed unequivocal identification of the calcium ATPase. Gold particles of 1 nm were successfully visualized in unstained or lightly stained sections and the density of labeling was about 20 times greater than with 10-nm gold. The average densities in areas of intense labeling were 2878 +/- 139/microns 2 with 5-nm gold and 4310 +/- 276/microns 2 with 1-nm gold. These numbers are similar to the density of particles in freeze-fracture replicas of sarcoplasmic reticulum. The low density of 10-nm gold suggests that the large gold particles hinder binding of secondary to primary antibodies. The difference between 1- and 5-nm gold is explained by the amounts of gold conjugated to the immunoglobulin. The results suggest that there is a one-to-one relationship between secondary immunoglobulins (1-nm or 5-nm gold conjugates) and oligomeric complexes of calcium ATPase.

Animals↗
PubMed1999

Nuclear localization of gold labeled-hydrocortisone-bovine serum albumin conjugate injected intravenously into the hormone-target cells of rat.

We have suggested in a previous study using 2-nm colloidal gold labeled-testosterone-bovine serum albumin (testosterone-BSA-gold) that 2-nm gold labeled-steroid hormone-BSA conjugates would be a useful tool for analyzing the mechanism of steroid hormone action (39). In this study, we examined whether hydrocortisone-BSA conjugate (hydrocortisone-BSA) showed a similar distribution to radiolabeled hydrocortisone in vivo, by injecting 2-nm colloidal gold labeled-hydrocortisone-BSA (hydrocortisone-BSA-gold) into the rat tail vein. The hydrocortisone-BSA-gold with silver enhancement became visible as silver deposits under electron microscopy in the nuclei of hepatocytes and hepatic stellate cells but not in Kupffer cells in the liver, and in the thymocytes and thymic reticuloepithelial cells in the thymus of a rat killed 2 h postinjection. The percentage of nuclei showing deposits in the non-target cells, the epithelial cells of the seminal vesicle, was similar to the value in the seminal vesicle of a control rat injected with BSA labeled with 2-nm colloidal gold as reported previously. In the hepatocytes and thymocytes of a control rat not injected, the percentages of nuclei showing deposits were similar to those in the rat injected with testosterone-BSA-gold or BSA-gold as reported previously, but lower than those in the rat injected with hydrocortisone-BSA-gold. These results suggest that hydrocortisone-BSA-gold is useful for the morphological study of hydrocortisone target cells, and imply that BSA conjugated with hydrocortisone can enter the target cell nuclei of the rat. The present study further indicates that the fate of gold labeled-steroid hormone-BSA conjugates may be decided at the cell membrane level.

Animals↗