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At least 19 recordsLinked to original sources

PubMed1992

Immunomodulatory effects of therapeutic gold compounds. Gold sodium thiomalate inhibits the activity of T cell protein kinase C.

Previous studies have shown that the gold compounds, gold sodium thiomalate (GST) and auranofin (AUR), which are effective in the treatment of rheumatoid arthritis, inhibit functional activities of a variety of cells, but the biochemical basis of their effect is unknown. In the current studies, human T cell proliferation and interleukin 2 production by Jurkat cells were inhibited by GST or AUR at pharmacologically relevant concentrations. Because it has been documented that protein kinase C (PKC) is involved in T cell activation, the capacity of gold compounds to inhibit PKC partially purified from Jurkat cells was assayed in vitro. GST was found to inhibit PKC in a dose-dependent manner, but AUR caused no significant inhibition of PKC at pharmacologically relevant concentrations. The inhibitory effect of GST on PKC was abolished by 2-mercaptoethanol. To investigate the effect of GST on the regulation of PKC in vivo, the levels of PKC activity in Jurkat cells were examined. Cytosolic PKC activity decreased slowly in a concentration- and time-dependent manner as a result of incubation of Jurkat cells with GST. To ascertain whether GST inhibited PKC translocation and down-regulation, PKC activities associated with the membrane and cystosolic fractions were evaluated after phorbol myristate acetate (PMA) stimulation of GST incubated Jurkat cells. Translocation of PKC was markedly inhibited by pretreatment of Jurkat cells with GST for 3 d, but the capacity of PMA to down-regulate PKC activity in Jurkat cells was not altered by GST preincubation. The functional impact of GST-mediated downregulation of PKC in Jurkat cells was examined by analyzing PMA-stimulated phosphorylation of CD3. Although GST preincubated Jurkat cells exhibited an increased density of CD3, PMA-stimulated phosphorylation of the gamma chain of CD3 was markedly inhibited. Specificity for the inhibitory effect of GST on PKC was suggested by the finding that GST did not alter the mitogen-induced increases in inositol trisphosphate levels in Jurkat cells. Finally, the mechanism of the GST-induced inhibition of PKC was examined in detail, using purified PKC subspecies from rat brain. GST inhibited type II PKC more effectively than type III PKC, and also inhibited the enzymatic activity of the isolated catalytic fragment of PKC. The inhibitory effect of GST on PKC activity could not be explained by competition with phospholipid or nonspecific interference with the substrate. These data suggest that the immunomodulatory effects of GST may result from its capacity to inhibit PKC activity.

Auranofin↗

PubMed2000

A review of controlled clinical trials examining the effects of antimalarial compounds and gold compounds on radiographic progression in rheumatoid arthritis.

At least 8 randomized controlled clinical trials have examined the effects of chloroquine or hydroxychloroquine on radiographic progression in rheumatoid arthritis (RA). At least 12 randomized controlled trials have examined the effects of either intramuscular or oral gold on radiographic progression. A review of these studies shows that hydroxychloroquine and chloroquine have minimal, if any, inhibitory effects on radiographically documented progression of bone erosions and joint destruction when used to treat RA. Intramuscular gold (with most of the data from studies of sodium aurothiomalate) appears to be better than placebo, about equal to intramuscular methotrexate (MTX), but probably not as effective as cyclophosphamide or azathioprine in its effects on radiographic progression. Auranofin appears to be better than placebo, comparable to or perhaps moderately less effective than intramuscular gold, comparable to lower dose oral MTX (7.5 mg/week), and not as effective as higher dose oral MTX (7.5-15 mg/wk) in inhibiting radiographic progression in RA. The inhibitory effects of gold compounds on proinflammatory cytokine synthesis (especially interleukin 1) offer a plausible mechanism for their inhibitory effects on bone erosion and joint destruction in RA.

Antimalarials↗

PubMed1977

Inhibition of antigen- and mitogen-induced human lymphocyte proliferation by gold compounds.

Gold sodium thiomalate (GST) inhibited in vitro antigen- and mitogen-triggered human lymphocyte DNA synthesis. Inhibition of responsiveness was observed with concentrations of GST equivalent to gold levels found in serum or tissues of patients receiving chrysotherapy, Inhibition was dependent upon the gold ion itself since GST and gold chloride were both inhibitory whereas thiomalic acid was not. Inhibition could not be explained by nonspecific killing of cells or by an alteration in the kinetics of the responses. GST inhibited mitogen-induced proliferation most effectively when present from the initiation of culture and could not inhibit the responsiveness of cells which previously had been activated by concanvalin A. These findings indicated that GST blocked a critical early step in lymphocyte activation. The degree of GST-induced inhibition of proliferation was increased in cultures of cells partially depleted of monocytes. Moreover, inhibition was reversed by supplementation of these cultures with purified monocytes. These observations suggested that GST blocked thymus-derived (T)-lymphocyte activation by interfering with a requisite function of the monocyte population in initiating such responses. Prolonged incubation of peripheral blood mononuclear cells with GST resulted in diminished mitogen responsiveness upon subsequent culture in the absence of gold. The addition of fresh monocytes restored responsiveness to these populations. Furthermore, preincubation of purified monocytes with GST rendered them deficient in their ability to support mitogen-induced T-lymphocyte proliferation on subsequent culture. These observations indicate that the major effect of GST results from interference with the functional capability of the monocyte population.

Antigens↗

PubMed1987

Regulation of heme metabolism and monooxygeneses in liver and kidney: influence of therapeutically used gold compounds.

Two gold compounds, gold sodium thiomalate (AuTM) and auranofin (AF) are presently in clinical use in therapy of rheumatoid arthritis. The effects of varying doses of AF administered to rats by either the p.o. or the i.p. route on heme metabolism were determined. Twenty four hours after a single dose of AF, decreases in the sulfhydryl-containing enzymes, delta-aminolevulinic acid dehydratase and ferrochelatase activities were observed in the liver and kidneys. These decreases in heme biosynthetic enzymes were accompanied by decreases in cytochrome P-450-dependent enzymic activities and increases in microsomal heme oxygenase activity. These changes were observed with AF dosages as low as 5 mg/kg, with maximal changes occurring at a p.o. dose of about 15 mg of AF per kg and an i.p. dose of 5 to 10 mg of AF per kg. Dose-response studies with AuTM showed that maximal changes in heme metabolism occur at a lower dose of AF than of AuTM, even though AF was administered p.o. and AuTM was administered parenterally. In addition, the kidneys appeared to be more susceptible to the inhibitory effects of the two chrysotherapeutic agents than did the liver. The present studies demonstrate the p.o. drug AF affects heme metabolism in a manner similar to that reported previously with the parenterally administered AuTM.

Animals↗

PubMed1984

[The pharmacology of gold compounds].

Parenterally administered gold compounds have been used for decades for treatment of rheumatoid arthritis. The new gold compound triethylphosphine gold (auranofin) can be partially absorbed in the gut following oral administration due to its higher lipophilic nature. This is probably also the main cause for the differences in kinetic properties versus the parenteral gold compounds. Following administration of auranofin, there are lower concentrations of gold in blood and organs; 95% of the gold is excreted in feces whereas 70% of gold, following gold sodium thiomalate, is excreted in the urine. These differences have consequences for the mode of adverse reactions. A common property of all gold compounds, however, is the relative distribution in organs. The highest concentrations of gold were found in the reticuloendothelial system, in liver, kidney and spleen, followed by joints. The mode of action of gold compounds is still unexplained. They inhibit some types of experimental inflammation and the activity of various cells involved in inflammatory processes. In some cases auranofin exerts a higher influence. Following incorporation of gold in lysosomes, the impairment of macrophage function appears to be most important. This effect probably influences (indirectly) the immune system since macrophages interact with T- and B-lymphocytes. The significance of these findings for the therapeutic effect of gold compounds is, however, not known. The rate of undesirable effects of gold compounds is very high requiring exact supervision during chrysotherapy. Mucosal and cutaneous reactions are very frequent, followed by proteinuria, diarrhea and thrombocytopenia. Bone marrow aplasia is most serious but relatively rare.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Distribution of gold in serum erythrocytes and white blood cells after in vitro incubation and during chrysotherapy with different gold compounds.

We examined the binding of gold to serum proteins and the gold level in serum and in blood cells both after incubation in vitro and under longterm treatment with 3 gold compounds. Gold was measured by atomic absorption spectrophotometry, a serum fractionated by gel chromatography; blood cells were separated by gradient centrifugation, and intracellular gold was measured after pressure decomposition and MIBK-extraction. Aurothiomalate (GSTM), gold keratinate (GK), and auranofin (AF) were used. AF showed the highest binding to globulins in in vitro and in vivo. With GSTM and GK there were no measurable amounts of gold in the red cell lysate or erythrocyte membranes whereas with AF 40% of gold was localized within erythrocytes. The amount of gold in granulocytes and mononuclear cells after incubation with AF is considerably higher than with GK and GSTM.

Auranofin↗

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↗

PubMed1979

Inhibition of pokeweed mitogen-induced immunoglobulin production in humans by gold compounds.

The effect of gold compounds on an in vitro model of antibody production was investigated. Peripheral blood mononuclear cells from healthy adult individuals were stimulated with pokeweed mitogen (PWM) and generation of immunoglobulin secreting cells (ISC) was assayed. Addition of gold sodium thiomalate 10 microgram/ml markedly inhibited mitogen-induced ISC production. The suppression of Ig production could not be explained by nonspecific lymphocyte toxicity or interference with the assay system. Inhibition of PWM responsiveness was mediated directly by the gold moiety and was not a function of the thiomalate. Furthermore, it was shown that maximum suppression of ISC generation occurred only when gold was added to cultures within the first 24 hours of incubation. This suggested that gold compounds inhibit an early step in B cell activation and differentiation rather than merely blocking Ig secretion by mature plasma cells.

Antibody-Producing Cells↗

PubMed1996

Injectable gold compounds: an overview.

Injectable gold compounds have enjoyed widespread, but occasionally controversial, use in rheumatoid arthritis since the 1920s. This overview examines the data from controlled trials and longer-term observational studies. We conclude that gold is equivalent to other widely used second-line agents in terms of efficacy. Toxicity profiles are similar, apart from methotrexate. It is most efficacious and toxic in the first 2 yr of treatment. There appears to be a dose-response relationship for both efficacy and toxicity. Gold is one of the few agents that decreases the rate of progression of erosions (RR 0.38, 95% CI 0.23-064). Gold compounds, therefore, have a definite place in the rheumatologist's armamentarium, but further research is required to determine optimal monitoring regimes as well as the role of maintenance therapy and combination therapy.

Antirheumatic Agents↗

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↗

PubMed1985

Effects of coordinated gold compounds on in vitro and in situ DNA replication.

Auranofin, a coordinated gold compound, inhibits in vitro DNA synthesis and displays in vivo antitumor activity. To understand the mechanisms of inhibition of DNA replication, we have examined the effects of auranofin and other gold complexes on the activities of purified cellular and herpesvirus-induced DNA polymerases, and on in situ DNA replication in permeabilized S phase KB cells. Evaluation of the data suggests the following conclusions. (1) The gold compounds varied in their abilities to inhibit DNA polymerase activities. DNA polymerase alpha was more sensitive to inhibition by gold compounds than DNA polymerase beta; (2) Inhibition of purified DNA polymerases by gold (I) compounds was noncompetitive with both DNA template and triphosphate substrates. Inhibition by SKF 101675, a gold (III) complex was competitive with DNA. (3) None of the gold compounds tested preferentially inhibited herpesvirus-induced DNA polymerases. (4) The gold complexes that inhibited in vitro DNA replication also inhibited in situ DNA synthesis. However, the potency and order of potency of the compounds varied between the in vitro and in situ systems. (5) Auranofin and other gold compounds inhibited the clonogenic capacity of KB cells in a concentration-dependent manner. The IC50 values measured in the clonogenic assay were significantly lower than those obtained from the in vitro and in situ DNA replication assays.

Anti-Inflammatory Agents↗

PubMed1996

Inhibition of human B cell activation by gold compounds.

The mechanism of action of gold compounds, which are effective in the treatment of rheumatoid arthritis (RA), has not been clearly identified. Although one of the characteristic features of RA is chronic stimulation of B cells, the effects of gold compounds on B cells have not been precisely assessed. We therefore examined the effects of gold sodium thiomalate (GST) on human B cells. IgM production was induced from highly purified B cells obtained from healthy donors by stimulation with Staphylococcus aureus Cowan 1 (SA) plus IL-2. T cell proliferation and IFN-gamma production were induced from highly purified T cells by stimulation with immobilized mAb to CD3. As little as 0.1 microg/ml (0.25 microM) GST almost completely suppressed B cell IgM production, whereas it did not suppress T cell proliferation or IFN-gamma production. The inhibition of IgM production by GST is not due to its thiomalate, but is most likely due to its gold components, since thiomalate alone did not inhibit IgM production. GST was required at the initiation of cultures to exert optimal suppressive effects on IgM production. Moreover, GST suppressed the expression of IL-2R (CD25) and transferrin receptor (CD71) on SA-stimulated B cells. These results indicate that GST preferentially inhibits the function of B cells at concentrations much lower than those which inhibit the function of T cells by interfering with the initial activation of B cells. The direct inhibitory effects of GST on human B cell activation described here may contribute at least in part to its therapeutic effect in RA.

Arthritis, Rheumatoid↗

PubMed1977

Aurosomes produced in the synovial membrane by the oral administration of a gold compound SK & F 36914.

Chlorotriethylphosphine gold (SK & F 36914) administered orally to rabbits produced aurosomes in the synovial membrane. These aurosomes were similar to aurosomes produced by parenteral or intra-articular injections of soluble gold salts such as sodium aurothiomalate and aurothioglucose. This study shows, (1) that an orally administered gold compound is capable of producing gold deposits in the synovial membrane, and (2) that such compounds may have a future in the treatment of rheumatoid arthritis.

Administration, Oral↗

PubMed2006

Sublethal concentrations of diverse gold compounds inhibit mammalian cytosolic thioredoxin reductase (TrxR1).

UNLABELLED: Thioredoxin reductase (TrxR) reduces thioredoxin (Trx), thereby contributing to cellular redox balance, facilitating the synthesis of deoxy-ribose sugars for DNA synthesis, and regulating redox-sensitive gene expression. Auranofin is a gold compound that potently inhibits TrxR. This inhibition is one suspected mechanism of auranofin's therapeutic benefit in the treatment of rheumatoid arthritis. The use of other gold compounds to treat cancer or inflammatory disease may rely on their ability to inhibit TrxR. In the current study, we tested the hypothesis that a variety of gold compounds may inhibit TrxR. METHODS: We exposed rat-TrxR1 to auranofin, gold sodium thiomalate, sodium aurothiosulfate, triphenyl phosphine gold chloride, or gold acetate, and measured TrxR activity ex vivo. We then compared TrxR1 inhibitory levels of gold compounds to those that inhibited mitochondrial activity of THP1 monocytes and OSC2 epithelial cells, estimated by succinate dehydrogenase activity. RESULTS: All gold compounds inhibited TrxR1 at concentrations ranging from 5 to 4000 nM (50% inhibitory concentration). The oxidation state of gold did not correlate with inhibitory potency, but ligand configuration was important. Au(I)-phosphine compounds (triphenyl phosphine gold chloride and auranofin) were the most potent inhibitors of TrxR. All TrxR1 inhibitory concentrations were sublethal to mitochondrial activity in both THP1 and OSC2 cells. CONCLUSIONS: Diverse types of gold compounds may be effective inhibitors of TrxR1 at concentrations that do not suppress cellular mitochondrial function. Inhibition may be optimized to some degree by altering the ligand configuration of the compounds. These results support future study of a variety of Au compounds for therapeutic development as inhibitors of TrxR1.

Animals↗

PubMedDate not supplied

Mechanism of action, pharmacology, clinical efficacy and side effects of auranofin. An orally administered organic gold compound for the treatment of rheumatoid arthritis.

The mechanism of action of auranofin, an oral organic gold compound used in the treatment of rheumatoid arthritis, is probably similar to the previously available parenteral gold compounds. Auranofin affects polymorphonuclear cells and monocytes at lower concentrations than gold sodium thiomalate and generally affects humoral and cell-mediated immunity in the same direction as the latter drug. The pharmacokinetics of auranofin are different from the intramuscular gold compounds. Auranofin is 20-25% orally absorbed and has less total body retention, greater fecal excretion, and less urinary excretion than gold sodium thiomalate. This may be due in part to its differing chemistry, including its lipophilicity and monomeric structure (at least in vitro). While many clinical studies are not yet complete, auranofin (6 mg/day) is clearly more effective than placebo for treating rheumatoid arthritis. Its efficacy relative to gold sodium thiomalate is not clear. Auranofin may be slightly less effective than gold sodium thiomalate, but because it is generally less toxic than intramuscular gold compounds, its therapeutic index may be more favorable.

Administration, Oral↗

PubMed1982

Correlation of in vitro and in vivo effects of gold compounds on leukocyte function: possible mechanisms of action.

The anti-inflammatory effects of gold compounds include suppression of PMN lysosomal enzyme release. Since lysosomal products can provoke PMN aggregation, we assessed the effect of two gold compounds, auranofin and GST, on suppressing aggregation, degranulation, and metabolic functions of the cells. Aggregation of 1 x 10(7) cytochalasin B-treated PMNs in response to 2 x 10(-7)M FMLP, as assessed by light scattering, was inhibited in a dose-dependent fashion by both drugs. Concentrations of auranofin ranging from 5 to 20 microM caused 30.8% to 89% inhibition, whereas 200 microM GST reduced aggregation by only 32%. FCS or BSA added to suspensions of normal PMNs considerably reduced the gold compound inhibitory effect on PMN aggregation. Cell viability assessed by dye exclusion and lactate dehydrogenase release was unaffected by the drugs. The suppressive activities of the drugs could not be removed by washing the PMNs. Correspondingly, the drugs suppressed lysosomal enzyme release induced by FMLP of PMNs rendered secretory with cytochalasin B. Concentrations of 20 microM auranofin and 200 microM GST resulted, respectively, in a 61.5% and 19.3% reduction of release of lysozyme, 61.7% and 27.1% reduction of beta-glucuronidase, 84.8% and 33.7%s reduction of myeloperoxidase, and 50.0% and 25.0% reduction of lactoferrin. Furthermore, auranofin inhibited 14C-1-glucose oxidation through the hexose monophosphate shunt in response to stimulation by either PMA or methylene blue. The in vivo studies suggested that auranofin could prevent neither neutropenia induced by zymosan-activated serum nor a corresponding rise in plasma lactoferrin levels. These findings suggest that the beneficial effect of gold compounds in rheumatoid arthritis are unlikely to be related to their ability to dampen PMN activation in vivo.

Animals↗

PubMed2003

Gold compound auranofin inhibits IkappaB kinase (IKK) by modifying Cys-179 of IKKbeta subunit.

Antirheumatic gold compounds have been shown to inhibit NF-kappaB activation by blocking IkappaB kinase (IKK) activity. To examine the possible inhibitory mechanism of gold compounds, we expressed wild type and mutant forms of IKKalpha and beta subunits in COS-7 cells and determined the effect of gold on the activity of these enzymes both in vivo and in vitro. Substitution of Cys-179 of IKKbeta with alanine (C179A) rendered the enzyme to become resistant to inhibition by a gold compound auranofin, however, similar protective effect was not observed with an equivalent level of IKKalpha (C178A) mutant expressed in the cells. Auranofin inhibited constitutively active IKKalpha and beta and variants; IKKalpha (S176E, S180E) or IKKbeta (S177E, S181E), suggesting that gold directly cause inhibition of activated enzyme. The different inhibitory effect of auranofin on IKKalpha (C178A) and IKKbeta (C179A) mutants indicates that gold could inhibit the two subunits of IKK in a different mode, and the inhibition of NF-kappaB and IKK activation induced by inflammatory signals in gold-treated cells appears through its interaction with Cys-179 of IKKbeta.

Amino Acid Substitution↗

PubMed1993

Suppression of interleukin-2 and interleukin-2 receptor biosynthesis by gold compounds in in vitro activated human peripheral blood mononuclear cells.

OBJECTIVE: To further investigate the mechanism of action of gold compounds by studying their effects on interleukin-2 (IL-2) and IL-2 receptor (IL-2R) biosynthesis. METHODS: We cultured phytohemagglutinin- or anti-CD3 antibody-activated normal peripheral blood mononuclear cells (PBMC), as well as the erythroleukemic K562 cell line, in the presence of gold sodium thiomalate or auranofin. Tritiated thymidine incorporation assays, cytotoxicity assays, immunofluorescence analysis, enzyme-linked immunosorbent assay, Northern blot, and RNA dot-blot hybridization were used. RESULTS: Gold compounds, at concentrations attainable in vivo, inhibited the proliferation of normal PBMC, with no evidence of direct cytotoxicity. This inhibitory effect was associated with a dose-dependent suppression of both IL-2 and IL-2R messenger RNA accumulation. In contrast, the same concentrations of gold compounds failed to inhibit the spontaneous proliferation of the IL-2-independent K562 cells. CONCLUSION: Our findings suggest an IL-2/IL-2R-mediated mechanism for suppression of lymphocyte proliferation by gold compounds, which might account for the immunomodulatory effects of gold in patients with rheumatoid arthritis.

Antibodies↗