Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes effects of sulphasalazine, 5-amino-salicylic acid (5-ASA) and sulphapyridine on polymorphonuclear neutrophils. Chemotaxis by polymorphonuclear neutrophils incubated with 5-ASA was reduced in a concentration dependent fashion (10(-5)-10(-4) M). Degranulation and release of lysozyme and beta-glucuronidase by activated polymorphonuclear neutrophils was inhibited by sulphasalazine but inhibited by sulphasalazine (IC50: 2 x 10(-4) M) and to a lesser extent by 5-ASA (IC50: 10(-3) M). Using a cell-free system sulphasalazine was found to be a strong scavenger and 5-ASA and sulphapyridine had only weak effects. Superoxide anion production requires translocation of a cytochrome b-245 and this translocation was reduced by sulphasalazine (P less than 0.01) but not by 5-ASA or sulphapyridine. In conclusion, the intact sulphasalazine molecule has an action of its own and marked differences exist between the action of sulphasalazine and 5-ASA, which may be important for the clinical activity.
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PMID:Effects of sulphasalazine and its metabolites on neutrophil chemotaxis, superoxide production, degranulation and translocation of cytochrome b-245. 168 23

Lysosomal preparations were exposed to various concentrations of dimethylsulphoxide (DMSO) and aspirin singularly and in combination. Acid phosphatase and beta-glucuronidase activities were measured and utilized as an indication of lysosomal membrane stability under experimental conditions in the presence and absence of these drugs. Extremely low concentrations of each drug were employed in an attempt to mimic the levels which might be feasible in vivo. There was a significant decrease of enzyme activity (increased structure-linked latency) in the presence of DMSO. Aspirin had no significant effect on the latency of the lysosomes. There was no indication of synergism between DMSO and aspirin. It was concluded that some of the therapeutic advantages attributed to DMSO in the treatment of arthritis and other musculoskeletal diseases may come from the stabilization of lysosomes in cells that contribute to the pathological condition. Aspirin did not seem to exert a therapeutic effect through this mechanism.
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PMID:The effects of aspirin and dimethyl sulphoxide on the latency of lysosomes in a cell-free system. 672 49

Endotoxic shock is associated with increased metabolism of arachidonic acid to thromboxanes (TX) and prostaglandins (PG). This study assessed the effects of varied doses of aspirin, an inhibitor of arachidonic acid metabolism, on Salmonella enteriditis endotoxin (20 mg/kg)-induced mortality, plasma levels of arachidonate metabolites and other pathophysiological sequelae in Long-Evans rats. Aspirin, in doses of 3.75, 15 an 30 mg/kg, given 30 min before endotoxin significantly (P less than .01) improved 24-hr survival from 11% to 60 to 70%, but 100 mg/kg afforded no protection. Pretreatment with aspirin (15 or 100 mg/kg) 30 min before endotoxin significantly (P less than .001) decreased the endotoxin-induced elevations in plasma levels of immunoreactive (i) TXB2, a stable metabolite of TXA2, i6-keto PGF1 alpha, a stable metabolite of PGI2 and significantly (P less than .05) inhibited thrombin-induced in vitro platelet iTXB2 synthesis. Endotoxin-induced hypoglycemia and elevations in serum acid phosphatase and beta-glucuronidase activities, lysosomal enzymes, were all significantly (P less than .01) attenuated by pretreatment with aspirin (15 mg/kg) 30 min before endotoxin. Aspirin (15 or 100 mg/kg) given 24 h before challenge with endotoxin significantly improved 24-hr survival to 42 (P less than .01) and 44% (P less than .005), respectively. Although 24 hr pretreatment with aspirin (15 or 100 mg/kg) significantly (P less than .001) reduced endotoxin-induced elevations in iTXB2, only the 100 mg/kg dose significantly lowered plasma levels of i6-keto PGF1 alpha. These observations are consistent with the notion that the beneficial effects of aspirin seen in experimental endotoxic shock may be mediated, in part, via reduction of platelet TXA2 synthesis.
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PMID:Protective effects of aspirin in endotoxic shock. 689 70