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The Yale Journal of Biology and Medicine Apr 1954
Topics: Animals; Aurothioglucose; Gold; Mice; Obesity
PubMed: 13169910
DOI: No ID Found -
Chemico-biological Interactions 1987The antirheumatic drug aurothioglucose is an inhibitor of the selenoenzyme GSH peroxidase. During chrysotherapy, the decreased levels of erythrocyte GSH and serum...
The antirheumatic drug aurothioglucose is an inhibitor of the selenoenzyme GSH peroxidase. During chrysotherapy, the decreased levels of erythrocyte GSH and serum sulfhydryls of rheumatoid arthritis patients are normalized concomitant with clinical efficacy. This investigation examined the in vivo and in vitro effect of gold(I) as aurothioglucose on enzymes related to the GSH redox cycle or metabolism. The enzymes measured were GSH peroxidase, GSSG reductase, gamma-glutamyl transpeptidase, gamma-glutamylcysteine synthetase, GSH S-transferase, GSH thiotransferase, glucose-6-phosphate dehydrogenase, superoxide dismutase and catalase. Rats were injected with 30 mumol aurothioglucose/kg body wt. daily for 7 days by intramuscular injection. GSH levels in aurothioglucose-treated rats were 68% higher in erythrocytes (P less than 0.005) and 45% higher in kidney (P less than 0.001) than in control rats. Treatment with aurothioglucose did not elevate plasma or liver GSH. The enzyme activities that were changed by aurothioglucose treatment were GSH peroxidase in kidney (41% decreased, P = 0.005) and liver (13% decreased, P less than 0.05), gamma-glutamyl transpeptidase in kidney (15% decreased, P less than 0.05), and catalase in kidney (58% decreased, P less than 0.001). Kidney glucose-6-phosphate dehydrogenase activity was increased 50% (P less than 0.005) and GSH S-transferase was increased 72% (P less than 0.001). In vitro the only liver enzymes inhibited more than 50% by concentrations of less than 50 microM aurothioglucose were GSH peroxidase (50% inhibited by 25 microM aurothioglucose) and GSH thiotransferase (50% inhibited by 5 microM aurothioglucose). Studies of in vitro enzyme inhibition by aurothioglucose could not be used to predict decreased enzyme activities in vivo. Although decreased activities of two major enzymes that utilize GSH, GSH peroxidase and gamma-glutamyl transpeptidase, coincided with elevated GSH in kidneys of aurothioglucose-treated rats, a direct cause and effect relationship remains speculative.
Topics: Animals; Aurothioglucose; Glutathione; Glutathione Peroxidase; Glutathione Transferase; Gold; Kidney; Lipid Peroxides; Liver; Male; Rats; Rats, Inbred Strains; Selenium
PubMed: 3121194
DOI: 10.1016/0009-2797(87)90064-0 -
The Journal of Nutrition Jan 1999Gold (I)-containing compounds, including aurothioglucose (ATG), are potent in vitro inhibitors of several selenocysteine-containing enzymes. Gold compounds have also...
Gold (I)-containing compounds, including aurothioglucose (ATG), are potent in vitro inhibitors of several selenocysteine-containing enzymes. Gold compounds have also been shown to potentiate the virulence of several viruses in mice, including coxsackievirus, implicated as a possible infectious agent in Keshan disease. One possible mechanism by which gold compounds may be increasing the virulence of viral infections in mice is by acting as a selenium antagonist in vivo and inducing oxidative stress. To investigate the possible role of gold compounds in inducing oxidative stress in mice, we assessed the ability of ATG administered in vivo to inhibit the activity of the selenocysteine-containing enzymes thioredoxin reductase (TR) and glutathione peroxidase (GPX1). Doses as low as 0. 025 mg ATG/g body weight caused significant and prolonged inhibition of TR activity in all tissues examined. No such inhibition of GPX1 activity was seen, indicating differential in vivo sensitivity of the enzymes to inhibition by ATG. In liver and heart, some recovery of TR activity was observed after a 7-d period, but no recovery was observed in pancreas or kidney. Because TR is involved in several important cellular redox functions, its inhibition most likely will affect multiple cellular processes. These results indicate that in vivo administration of ATG results in significant and long-lasting inhibition of TR activity. Such inhibition of TR could lead to increased levels of oxidative stress in vivo, thereby increasing the virulence of several viruses including the coxsackievirus.
Topics: Animals; Aurothioglucose; Dose-Response Relationship, Drug; Glutathione Peroxidase; Injections, Intraperitoneal; Male; Mice; Mice, Inbred C3H; Thioredoxin-Disulfide Reductase; Tissue Distribution
PubMed: 9915899
DOI: 10.1093/jn/129.1.194 -
Arthritis and Rheumatism Feb 1984
Topics: Adult; Arthritis, Rheumatoid; Aurothioglucose; Chemical and Drug Induced Liver Injury; Female; Gold; Humans; Liver; Liver Function Tests
PubMed: 6421293
DOI: 10.1002/art.1780270217 -
Chemical Reviews May 2023The gold drugs, gold sodium thiomalate (Myocrisin), aurothioglucose (Solganal), and the orally administered auranofin (Ridaura), are utilized in modern medicine for the... (Review)
Review
The gold drugs, gold sodium thiomalate (Myocrisin), aurothioglucose (Solganal), and the orally administered auranofin (Ridaura), are utilized in modern medicine for the treatment of inflammatory arthritis including rheumatoid and juvenile arthritis; however, new gold agents have been slow to enter the clinic. Repurposing of auranofin in different disease indications such as cancer, parasitic, and microbial infections in the clinic has provided impetus for the development of new gold complexes for biomedical applications based on unique mechanistic insights differentiated from auranofin. Various chemical methods for the preparation of physiologically stable gold complexes and associated mechanisms have been explored in biomedicine such as therapeutics or chemical probes. In this Review, we discuss the chemistry of next generation gold drugs, which encompasses oxidation states, geometry, ligands, coordination, and organometallic compounds for infectious diseases, cancer, inflammation, and as tools for chemical biology via gold-protein interactions. We will focus on the development of gold agents in biomedicine within the past decade. The Review provides readers with an accessible overview of the utility, development, and mechanism of action of gold-based small molecules to establish context and basis for the thriving resurgence of gold in medicine.
Topics: Humans; Auranofin; Arthritis, Rheumatoid; Anti-Inflammatory Agents; Gold; Aurothioglucose; Gold Sodium Thiomalate
PubMed: 37071737
DOI: 10.1021/acs.chemrev.2c00649 -
Zeitschrift Fur Rheumatologie Apr 2002We describe the case of a 78-year old woman, with rheumatoid arthritis, 3 years of regular parenteral gold administration and Chrysiasis. Chrysiasis is a rare permanent...
We describe the case of a 78-year old woman, with rheumatoid arthritis, 3 years of regular parenteral gold administration and Chrysiasis. Chrysiasis is a rare permanent pigmentation of the skin resulting from the parenteral administration of gold. The cause of the pigmentation is multifactorial and not fully established at the moment.
Topics: Aged; Antirheumatic Agents; Arthritis, Rheumatoid; Aurothioglucose; Female; Humans; Hyperpigmentation; Long-Term Care
PubMed: 12056295
DOI: 10.1007/s003930200026 -
Zeitschrift Fur Rheumatologie Oct 2001We describe the case of a 78-year old woman, with rheumatoid arthritis, 3 years of regular parenteral gold administration and Chrysiasis. Chrysiasis is a rare permanent...
We describe the case of a 78-year old woman, with rheumatoid arthritis, 3 years of regular parenteral gold administration and Chrysiasis. Chrysiasis is a rare permanent pigmentation of the skin resulting from the parenteral administration of gold. The cause of the pigmentation is multifactorial and not fully established at the moment.
Topics: Aged; Antirheumatic Agents; Arthritis, Rheumatoid; Aurothioglucose; Diagnosis, Differential; Facial Dermatoses; Female; Humans; Long-Term Care; Pigmentation Disorders
PubMed: 11759236
DOI: 10.1007/s003930170036 -
Recenti Progressi in Medicina Aug 1983
Topics: Arthritis, Rheumatoid; Auranofin; Aurothioglucose; Gold; Humans
PubMed: 6417742
DOI: No ID Found -
Scandinavian Journal of Rheumatology.... 1983In rheumatoid arthritis both lymphocyte-mediated and antibody-mediated immune reactions are important for the inflammatory lesions. In vivo activated B... (Comparative Study)
Comparative Study Review
In rheumatoid arthritis both lymphocyte-mediated and antibody-mediated immune reactions are important for the inflammatory lesions. In vivo activated B lymphocytes/plasma cells, T lymphocytes and monocytes/macrophages (Mo) are intimately involved in the disease process. Several clinical observations suggest an immunosuppressive action of gold salts. In humans, gold salts interfere with a number of Mo functions in vitro, including cellular interactions between Mo and T lymphocytes. Some workers have shown that the activation of human T lymphocytes is inhibited by gold salts, most probably secondary to an inhibition of Mo-T cell cooperation. Recent experiments indicate that gold salts also affect the in vitro differentiation of human B lymphocytes in response to polyclonal activators. Both the gold atom and the SH group seem to be important for the immunosuppressive actions of gold salts.
Topics: Anti-Inflammatory Agents; Antibody Formation; Arthritis, Rheumatoid; Aurothioglucose; B-Lymphocytes; Gold; Gold Sodium Thiomalate; Humans; Immunity, Cellular; Leukocyte Migration-Inhibitory Factors; Monocytes; Penicillamine; T-Lymphocytes
PubMed: 6426050
DOI: 10.3109/03009748309095340 -
The Medical Journal of Australia Sep 1984Forty-three patients in whom treatment with sodium aurothiomalate was discontinued because of adverse reactions that either were relatively severe or recurred on...
Forty-three patients in whom treatment with sodium aurothiomalate was discontinued because of adverse reactions that either were relatively severe or recurred on rechallenge received treatment with aurothioglucose in oily base. Thirty-six of them had rheumatoid arthritis, four had psoriatic arthritis and three had juvenile chronic arthritis. Aurothioglucose therapy was introduced cautiously and increased gradually to a maintenance regimen, usually 5-20 mg/week, administered by intramuscular injection. The clinical response was good in 25 patients (60%), 14 of whom continued to receive aurothioglucose therapy on a long-term basis. Adverse reactions to aurothioglucose developed in 17 patients (40%); these were generally mild, and, in all but four patients, were of the same type as those induced by sodium aurothiomalate therapy. Results show that aurothioglucose in oily base may be successfully administered in a low-dose regimen to selected patients who are intolerant of sodium aurothiomalate.
Topics: Arthritis, Rheumatoid; Aurothioglucose; Drug Tolerance; Gold; Gold Sodium Thiomalate; Humans; Injections, Intramuscular; Time Factors
PubMed: 6438454
DOI: No ID Found