Disease relevance of (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• Obesity was induced by aurothioglucose [1].
• 4. Auranofin (0.5 to 50 microM), a chrysotherapeutic agent with antiproliferative properties used for treating rheumatoid arthritis, also markedly inhibited the EGF-URO response; however, other gold-containing compounds (aurothioglucose or gold sodium thiomalate at 30 to 100 microM) failed to cause significant inhibition [2].
• Anti-rheumatic compound aurothioglucose inhibits tumor necrosis factor-alpha-induced HIV-1 replication in latently infected OM10.1 and Ach2 cells [3].
• The other causes of death could be classified into cancer, sepsis, amyloidosis, leukaemia, renal insufficiency of unknown cause, perforation of the oesophagus, probably related to the treatment with non-steroidal anti-inflammatory drugs, and pancytopenia during aurothioglucose treatment [4].
• Hydrocortisone, triamcinolone acetonide, aurothioglucose and soybean trypsin inhibitor were added to normal human skin explants cultured with IgG from pemphigus serum to determine if acantholysis could be prevented [5].

High impact information on (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• In vitro IKK activity was suppressed by addition of hydrophilic gold compounds, such as aurothiomalate, aurothioglucose, and AuCl3 [6].
• Specificity for thioredoxin reductase was indicated by loss of activity in dialyzed cytosol prepared from livers of selenium-deficient rats, by inhibition with aurothioglucose at concentrations selective for thioredoxin reductase, and by stimulation with selenocystine [7].
• By Northern blot analysis, both reg I and reg II mRNAs are detected in the normal pancreas and hyperplastic islets of aurothioglucose-treated mice, but not in the normal islets [8].
• Aurothioglucose (Solganal), rarely produces vasomotor reactions, and may be preferred to GST in elderly RA patients with concomitant cardiovascular disease or atherosclerosis [9].
• Rats treated with aurothioglucose for 3 days exhibited a significant decrease in 5'-MD activity in liver and kidney microsomes, whereas the tissue content of 5'-MD was not affected [10].

Chemical compound and disease context of (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• HLA-DR antigens and proteinuria induced by aurothioglucose and D-penicillamine in patients with rheumatoid arthritis [11].
• The effects of the antiarthritic drugs aurothiomalate (AuTm), aurothioglucose (AuTg), auranofin, its metabolite triethylphosphinegold(I)thioglucose (Et3PAuTg), and several related complexes on the growth of Pseudomonas putida were studied [12].
• Treatment with aurothioglucose (1 mg/kg, IM, q 7 d) that was initiated during administration of prednisolone and was continued after discontinuation of corticosteroid administration failed to prevent redevelopment of pemphigus foliaceus [13].

Biological context of (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• Aurothioglucose, an inhibitor of thioredoxin reductase, reduces the rate of As methylation by rrcyt19 in thioredoxin-supported reactions [14].
• Aurothioglucose, an inhibitor of selenocysteine enzymes, inhibited DIF-1 3(5)-dechlorinase with IC50 = 100 nM [15].
• Effects of aurothioglucose on iron-induced rat liver microsomal lipid peroxidation [16].
• Aurothioglucose (ATG) is presently employed both by clinicians in the treatment of advanced rheumatoid arthritis and by neuroscience researchers to generate lesions around the circumventricular organs (CVOs) of rodent brains, resulting in obese animals [17].
• In contrast, aurothioglucose was less effective than AF in inhibiting epinephrine- or collagen- induced platelet aggregation [18].

Anatomical context of (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• Treatment of HepG2 or H4IIE cultured liver cells for 48 h with sodium selenite (0-116 nmol/l) tripled the activity of the selenoenzyme TR, measured as aurothioglucose-sensitive dehydroascorbic acid (DHA) reduction [19].
• Low-dose electron microscopy has been used to obtain images of two-dimensional crystals of this channel (produced by treating outer membranes from fungal mitochondria with phospholipase A2) embedded in vitreous ice or aurothioglucose [20].
• Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucose [21].
• During 20 weeks of aurothioglucose therapy, gold in a mother's serum and breast milk and her nursing infant's serum and urine were measured [22].
• The progression of neuronal, myelin, astrocytic, and immunological changes in the rat brain following exposure to aurothioglucose [17].

Associations of (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol with other chemical compounds

• 3 Crude cathepsin preparations were activated by low concentrations of dithiothreitol and also by aurothioglucose, due to the displacement of an inhibitor [23].
• The activity of the purified enzyme was monitored by the NADPH-dependent reduction of 5, 5'-dithiobis(2-nitrobenzoic acid) (DTNB); this activity was fully inhibited by 1 microM aurothioglucose [24].
• Exposure of cultured hepatocytes to inorganic As(III) (iAs(III)), MAs(III), or aurothioglucose (ATG, a competitive inhibitor of TR activity) for 30 min caused a concentration-dependent reduction in TR activity [25].
• Sodium aurothiomalate and aurothioglucose selectively interfered with lymphocyte-mediated amplification of MCF release, whereas auranofin inhibited spontaneous production of monocytes and the action of MCF on synovial cells [26].
• We investigated glucose transporters (GLUT 1 and GLUT 4) in subcellular membrane fractions of white adipose tissue (WAT) of insulin-resistant obese aurothioglucose (AuTG)- or monosodium glutamate (MSG)-treated mice [27].

Gene context of (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• Aurothioglucose inhibits murine thioredoxin reductase activity in vivo [28].
• Effect of chronic aurothioglucose treatment of rats on kidney catalase and cytochromes [29].
• Gold salts, auranofin (AF), aurothiomalate (ATM) and aurothioglucose (ATG) displayed immunosuppressive action in a series of in vitro assays which mimic the cell-cell interactions thought to occur in rheumatoid arthritis [30].
• Treatment with NF-kappaB nuclear translocation inhibitor SN50 or thioredoxin reductase (TR) inhibitor aurothioglucose depressed this stimulatory action [31].
• Effects of aurothioglucose and dietary Se on glutathione S-transferase activities and glutathione concentrations in chick tissues [32].

Analytical, diagnostic and therapeutic context of (2R,3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• Of various treatments, administration of corticosteroids or injectable gold (aurothioglucose) proved most effective in controlling the clinical signs [33].
• Rats were injected with 30 mumol aurothioglucose/kg body wt. daily for 7 days by intramuscular injection [34].
• Animal experiments investigating damage to the liver, kidney and heart with Solganal showed no serious findings [35].
• Sixty male Swiss-Webster mice were given intraperitoneal injections of the gold-containing drug aurothioglucose in saline at 3 dose levels: 50, 200, and 400 mg/kg [36].
• Radiographic films of 40 patients participating in a single centre patient blind study of auranofin versus aurothioglucose were evaluated in a random order by one reader [37].

References