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At least 379 records · Page 21Linked to original sources
PubMed1990

The effect of antirheumatic drugs on interleukin 1 (IL-1) activity and IL-1 and IL-1 inhibitor production by human monocytes.

Interleukin 1 (IL-1) is an important mediator of immune regulation, inflammation and joint destruction in arthritis. The objective of our study was to investigate the effect of a number of representative antirheumatic agents on the activity of IL-1 and the production of both IL-1 and IL-1 inhibitor by human monocytes. IL-1 activity and production were measured by its effect on the proliferation of murine thymocytes; IL-1 inhibitor production was assayed by inhibition of IL-1 mediated thymocyte proliferation. Dexamethasone (10-100 nM) inhibited IL-1 production and IL-1 mediated thymocyte proliferation. High concentrations of indomethacin, aspirin, and 12 other nonsteroidal antiinflammatory drugs (NSAID) inhibited IL-1 activity, or production or both. Methotrexate inhibited IL-1 activity without affecting IL-1 production. D-penicillamine inhibited IL-1 activity and tended to inhibit IL-1 production. Gold compounds inhibited IL-1 activity, but only auranofin inhibited IL-1 production. Acetaminophen in high concentrations (1 mg/ml) inhibited IL-1 activity and production. Colchicine inhibited IL-1 activity but not IL-1 production. No drug tested induced, by itself, the production of IL-1 inhibitor or enhanced the production of IL-1 inhibitor.

Acetaminophen↗
PubMedDate not supplied

Lack of effect of gold salts on acetylcholine or histamine contraction of canine tracheal and bronchial smooth muscle.

In vitro gold salt incubation with proximal and distal canine airway smooth muscle was compared to untreated canine airway muscle with respect to histamine and acetylcholine-induced contraction. Gold chloride and gold sodium thiomalate had no effect on either proximal or distal canine airway smooth muscle agonist-induced contraction. Gold chloride in concentrations greater than 10(-5) M had a direct contractile effect. These results differ from previous studies which showed an inhibition of the histamine response of guinea-pig tracheal smooth muscle following in vitro preincubation with gold salts. This difference suggests that the mechanism(s) of the beneficial effects of long-term gold salt therapy on human asthma cannot be reliably studied with short-term in vitro animal preparations without first assessing species differences with respect to the effects of therapeutic agents. Human airway smooth muscle preparations would be the best means of addressing this question.

Acetylcholine↗
PubMedDate not supplied

Intestinal calcium absorption in rheumatoid arthritis. A study using whole body counting.

Conflicting results are reported in the literature concerning the changes in intestinal calcium absorption in rheumatoid arthritis (RA). In the present work, intestinal calcium absorption was studied in 27 postmenopausal women with RA, using whole body counting as the study method and orally administered Ca-47 as the tracer. Nobody was on corticosteroid therapy, but all received non-steroidal anti-inflammatory drugs and hydroxy chloroquine or gold compounds. The mean calcium absorption was 22.3% of the dose administered, with a standard deviation of 8.0%. The results obtained were not significantly different from those of 40 age- and sex-matched controls (mean +/- SD: 22.0% +/- 6.0%). Our findings seem to exclude the hypothesis of calcium malabsorption as one of the causes leading to osteoporosis in RA.

Aged↗
PubMedDate not supplied

Mechanisms of action of slow-acting drugs in rheumatoid arthritis.

Slow-acting anti-rheumatic drugs exhibit a number of similar properties in treated patients that suggest that they may have a common mode of action in rheumatoid arthritis. In vitro evaluation of drug action suggests that each of the slow-acting agents possesses immunosuppressive activity that may explain its therapeutic efficacy in rheumatoid arthritis. Even though these agents appear to be able to suppress immune responses, the site of action of these agents differs. Thus, gold compounds and the antimalarials suppress the activity of mononuclear phagocytes, whereas D-penicillamine and other thiol-containing slow-acting agents inhibit the activity of helper T cells. These agents may therefore be effective by interfering with various specific aspects of the immunologic reactivity that drives the chronic inflammation of rheumatoid arthritis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1989

Methotrexate in the treatment of rheumatoid arthritis.

Methotrexate is an effective agent for the treatment of rheumatoid arthritis. It is now widely prescribed for patients who have not tolerated or responded to gold compounds or penicillamine. Minor adverse reactions are common, and fatal pulmonary toxicity or cirrhosis can occur. The drug does not produce disease remissions, but continued administration helps reduce pain, stiffness and swelling. Within the past year, the Food and Drug Administration has approved methotrexate for use in treating rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1985

Effects of various inhibitors of arachidonic acid oxygenation on macrophage superoxide release and tumoricidal activity.

Macrophages release a variety of arachidonic acid metabolites after treatment with various membrane triggers or particulate stimuli. We examined the role of phospholipase and lipoxygenase inhibitors in the modulation of superoxide production and tumor cytolysis by murine macrophages. Superoxide was induced by the soluble stimulus, phorbol myristate acetate (PMA), and the particulate stimulus, opsonized zymosan, and was measured by the reduction of ferricytochrome c with the use of a micro ELISA reader. Macrophage-mediated tumor cytolysis was induced by hybridoma-derived, macrophage-activating factor (MAF) and was quantitated by 51Cr release from P815 target cells. In both assays, 72-hr peptone-elicited macrophages were used. Dexamethasone, and to a lesser degree hydrocortisone, inhibited superoxide release and MAF-induced tumor cytolysis. Inhibition in the superoxide assay required pretreatment with corticosteroid. Only the gold compound, auranofin, inhibited superoxide when given simultaneously with stimulant. Other phospholipase inhibitors, including mepacrine and 4-bromophenacyl bromide, and several lipoxygenase inhibitors, including BW755c, nordihydroguaiaretic acid (NDGA), and 5,8,11,14-eicosatetraynoic acid (ETYA), failed to modulate either macrophage response at nontoxic concentrations. At the concentrations tested in the tumoricidal and superoxide assays, mepacrine and 4-bromophenacyl bromide inhibited the release of 14C-arachidonic acid from macrophages stimulated with opsonized zymosan. Our data strongly suggest that corticosteroids suppress macrophage superoxide production and tumoricidal function by a nonphospholipase-dependent mechanism.

Animals↗
PubMed1985

In vitro inhibition of myelopoiesis by gold salts and D-penicillamine.

Leukopenia is one of the more serious side effects of gold and D-penicillamine therapy. We report that gold salts (gold thiomalate, gold chloride and gold thioglucose) and D-penicillamine suppressed the in vitro development of colonies of myeloid cells (macrophage, granulocyte and megakaryocyte) from progenitor cells in murine bone marrow; these drugs were also effective in inhibiting the development of macrophage and granulocytic colonies in human bone marrow. The drugs generally required concentrations of 10(-5) M in the murine system, whereas they were active at 10(-7)-10(-8) for the human progenitor cells. The disease suppressive activity of gold salts and D-penicillamine could result in part from the reduction of cell numbers in arthritic lesions; our findings would provide a mechanism for this possibility.

Animals↗
PubMedDate not supplied

[Liberation of the oxygen radical from peripheral human phagocytes (granulocytes and monocytes) in patients with chronic polyarthritis].

Monocytes from patients with definite or classical rheumatoid arthritis show a significantly higher release of O2-radicals in the chemiluminescence assay (2925 X 10(3) cpm) than those of healthy volunteers (267 X 10(3) cpm) (p = 0.01). This difference does not appear in a similar test with granulocytes, which in both groups tested show a mean chemiluminescence of 2739 X 10(3) and 2547 X 10(3) cpm. The chemiluminescence of monocytes is clearly time-course dependent: in the morning we saw the least response, at noon the highest. Following our results, corticosteroids lower chemiluminescence significantly (p = 0.05), while non steroidal antirheumatic drugs and long-term therapy with gold compounds, etc., do not affect chemiluminescence.

Arthritis, Rheumatoid↗
PubMed1983

Lichenoid eruption produced by captopril.

Captopril, an oral active dipeptidylcarboxypeptidase inhibitor with antihypertensive properties, has been reported to have the following cutaneous side effects: macular and papular skin eruptions, urticaria, angioedema, mouth ulcers, pemphigus, and pityriasis rosea-like eruptions. Here, to the best of our knowledge, is the first case in which a pityriasis rosea-like eruption evolved into a lichenoid drug eruption. Also discussed is the remarkable similarity in the side effects of captopril, gold compounds, d-penicillamine, and organic mercurials.

Captopril↗
PubMed1982

[Rheumatoid arthritis with antinuclear factor. A prospective study of 50 cases (author's transl)].

The clinical and laboratory features of rheumatoid arthritis (RA) with antinuclear factor (ANF) were prospectively analyzed in 50 patients and compared with those of another series of 50 patients of similar age, sex and duration of disease, but without ANF. The severity of articular lesions was about the same in both series, but systemic symptoms and Gougerot-Sjögren syndrome occurred more frequently in patients with ANF. Gold compounds and D-penicillamine appeared to be well tolerated by all patients. RA patients with ANF had more strongly positive responses to latex and Waaler-Rose tests. Farr's radioimmunoassay was sometimes positive (11/49), but as a rule, the degree of positivity was inferior to 50%.

Adult↗
PubMed1993

Colonic toxicity of administered medications and chemicals.

Although medication-induced colonotoxicity is uncommon, it is important that it be recognized, because the initial therapy for this condition is medication discontinuation. This review categorizes the association between the listed medications and colonotoxicity as "well-established" or "probable," according to the following criteria: number of clinical studies by independent clinical investigators, total number of reported cases, plausibility of an association based on experimental and pharmacologic studies, and validity of an association in each reported case. Medications associated with colonic ischemia include cocaine, ergotamine, estrogen, amphetamines, digitalis, methysergide, and vasopressin. Medications associated with colonic pseudoobstruction include narcotics, phenothiazines, vincristine, atropine or other anticholinergics, ganglionic blocking agents, and tricyclic antidepressants. Medications promoting infectious or necrotizing enterocolitis include numerous antibiotics associated with pseudomembranous colitis, deferoxamine associated with Yersinia enterocolitis, chemotherapy associated with neutropenic colitis, and hyperosmolar medications or formulas in infants. Medications associated with an allergic, inflammatory, or cytotoxic colitis include gold compounds, nonsteroidal antiinflammatory drugs, alpha-methyldopa, flucytosine, methotrexate, salicylates, and sulfasalazine. Potassium chloride, administered in slow-release wax matrices, can cause intestinal ulcers. Chronic cathartic use leads to colonic hypomotility and abdominal distention. Methysergide can cause a colonic stricture due to retroperitoneal fibrosis. Intrarectally administered compounds that have produced a toxic colitis include powerful acids, bases, and other corrosives. Enemas using hypertonic radiographic contrast agents have been associated with colitis in patients with colonic obstruction.

Colonic Diseases↗
PubMed1996

Treatment of HIV associated psoriatic arthritis with oral gold.

We report a patient with human immunodeficiency virus (HIV) infection and disabling psoriatic arthritis who was treated with auranofin. Her skin lesions and arthritis resolved after auranofin treatment and she has remained free of opportunistic infections during 24 mo followup. Her CD4 count during oral gold therapy showed a significant, sustained increase in CD4 cells. The literature on the effect of gold compounds on HIV infectivity and HIV reverse transcriptase is reviewed.

Adult↗
PubMedDate not supplied

[The antibacterial activity of preparations with highly dispersed iron].

High-dispersed magnetized iron preparations of various coercive force and its preparations with Ag, Au, Pt obtained by thermochemical method have been studied for their effect on plants and bacteria pathogenic for animals. It is established that magnetized iron intensifies antibacterial effect of certain metals. Of the studied preparations only high-dispersed Fe-Ag had distinctly expressed bactericidal effect. Other preparations had weak antibacterial effect or had not it at all. All the preparations have strong adsorption capacity.

Adsorption↗
PubMedDate not supplied

Analysis of treatment terminations with gold and antimalarial compounds in rheumatoid arthritis.

Life table analysis was used to determine the incidence of treatment termination in rheumatoid arthritis patients after initial therapeutic courses of gold (93) and antimalarial compounds (101). Patients treated with antimalarial compounds tended to terminate treatment sooner than those receiving gold. The most common reasons for discontinuing antimalarial therapy were lack of initial benefit and loss of response to the drug. Clinical and laboratory characteristics of patients at onset of therapy did not influence failure rates to a great extent.

Adult↗
PubMed1979

Gold and thiol compounds in the treatment of rheumatoid arthritis: excretory fate and tissue distribution of thiomalate in relation to gold after administration of myocrisin (auro-thiomalate).

Double isotope-labelled auro thiomalate (Au195-C14-thiomalate) has been administered to mice and rats, and the excretory fate and tissue distribution have been studied. The results show that the gold and the thiomalate separate in vivo resulting in protein-bound gold and release of free thiomalate. About half of this thiol is excreted in the urine during the first day and the remaining half is taken up by the tissues. Thiomalate penetrates cellular membranes poorly, but is able to interact slowly with proteins (mixed disulphide formation). Part of the thiomalate which remains in the body is membrane bound. In contrast to penicillamine little thiomalate remains in circulation a few hours after administration. Gas chromatography--mass spectrometry has been used to search for the presence of free thiomalate in rheumatoid arthritis patients on Myocrisin (auro thiomalate) therapy. Thiomalate was found in their urine, but not in serum and synovial fluid 20 hours after administration. As thiomalate is released in the body after administration of Myocrisin. the question arises whether this thiol, like penicillamine, may have a beneficial effect in the treatment of rheumatoid arthritis.

Animals↗
PubMed1997

A Novel Anionic Gold-Indium Cluster Compound: Synthesis and Molecular and Electronic Structure.

The insertion of InBr into the Au-Br bond of [(Ph(3)P)AuBr] in tetrahydrofuran (thf) in the presence of [(CH(2)PPh(2))(2)] (dppe) leads to the formation of an orange complex [(dppe)(2)Au](+)[(dppe)(2)Au(3)In(3)Br(7)(thf)](-), 2. Analytical, spectroscopic, and X-ray structural investigations showed that this product is an anionic analogue of a neutral chloride complex [(dppe)(2)Au(3)In(3)Cl(6)(thf)(3)], 1, prepared recently. Both complexes have an Au(3)In(3) cluster core of approximate C(2)(v)() symmetry with one extremely short Au-Au bond [Au1-Au3 2.575(1) Å] as part of a quasi-linear array P1-Au1-Au3-P4, suggesting the presence of a bis(phosphine) complex of the neutral Au(2) molecule as part of the cluster. The third gold atom (Au2) is then assigned oxidation state +1. To gain deeper insight into the structure and bonding of this novel class of gold cluster compounds, regarding mainly the peculiar cluster geometry, the charge distribution, and the oxidation states, a series of scalar relativistic all-electron density functional (DF) calculations on model systems has been performed. As a model for 1, the neutral cluster {Au(3)(PH(3))(4)[InCl(2)(H(2)O)](3)} was studied. For the examination of the geometry of complexes 1 and 2, the cluster Au(3)(PH(3))(4)I(3) has been considered as a further simplified model, where iodine replaces the InX(2)(thf) units. Experimental and calculated cluster geometries agree satisfactorily, and the formal oxidation states of the gold atoms (0 for Au1 and Au3, +1 for Au2) could be confirmed, but for the In centers no interpretable differences of the Mulliken charges were found.

Journal Article↗
PubMed2000

Evidence of gold-gold intra- and intermolecular interactions gained by laser desorption/ionisation and fast atom bombardment mass spectrometry in the study of some gold(I) coordination compounds

The mass spectrometric behaviour of some two-coordinated linear gold(I) complexes has been studied by fast atom bombardment (FAB) and laser desorption/ionisation (LDI) methods. The results obtained demonstrate some interesting aspects of Au-Au interactions. The detection under FAB conditions of Au(n)(+) clusters, in particular of Au(3)(+) species, can be rationalised by the presence of significant intramolecular Au-Au interactions, while the formation under LDI conditions of Au(n)(+) clusters can be considered indicative of Au(ellipsis)Au intermolecular interactions present in the solid state. Copyright 2000 John Wiley & Sons, Ltd.

Journal Article↗
PubMed2006

A novel anticancer gold(III) dithiocarbamate compound inhibits the activity of a purified 20S proteasome and 26S proteasome in human breast cancer cell cultures and xenografts.

Although cisplatin has been used for decades to treat human cancer, some toxic side effects and resistance are observed. It has been suggested that gold(III) complexes, containing metal centers isoelectronic and isostructural to cisplatin, are promising anticancer drugs. Gold(III) dithiocarbamate complexes were shown to exhibit in vitro cytotoxicity, comparable with and even greater than cisplatin; however, the involved mechanism of action remained unknown. Because we previously reported that copper(II) dithiocarbamates are potent proteasome inhibitors, we hypothesized that gold(III) dithiocarbamate complexes could suppress tumor growth via direct inhibition of the proteasome activity. Here, for the first time, we report that a synthetic gold(III) dithiocarbamate (compound 2) potently inhibits the activity of a purified rabbit 20S proteasome and 26S proteasome in intact highly metastatic MDA-MB-231 breast cancer cells, resulting in the accumulation of ubiquitinated proteins and the proteasome target protein p27 and induction of apoptosis. The compound 2-mediated proteasome inhibition and apoptosis induction were completely blocked by addition of a reducing agent DTT or N-acetyl-L-cysteine, showing that process of oxidation is required for proteasome inhibition by compound 2. Treatment of MDA-MB-231 breast tumor-bearing nude mice with compound 2 resulted in significant inhibition of tumor growth, associated with proteasome inhibition and massive apoptosis induction in vivo. Our findings reveal the proteasome as a primary target for gold(III) dithiocarbamates and support the idea for their potential use as anticancer therapeutics.

Acetylcysteine↗