Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney stones have an overall incidence of two to three percent in western countries. In many patients, the disease process is difficult to control and recurrence rates are high: 20 to 50 percent over the subsequent ten years. The pathogenesis and standard methods of treatment for the five major types of stones (i.e., calcium oxalate, struvite, calcium phosphate, uric acid, and cystine) are reviewed. Three new drugs are reviewed in the context of their roles in the selective treatment of kidney stones. Cellulose sodium phosphate (Calcibind) is a nonabsorbable ion-exchange resin with a limited indication for the treatment of calcium stones associated with absorptive hypercalciuria Type I. Acetohydroxamic acid (Lithostat) is an urease-inhibitor that is indicated as adjunctive therapy in patients with chronic urea-splitting urinary tract infections and struvite stones. Potassium citrate (Urocit) is an investigational agent that has clinical efficacy in patients with calcium oxalate and calcium phosphate stones who are hypocitraturic. In addition, potassium citrate is an alkalinizing agent that can be used in patients with uric acid stones.
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PMID:New drug therapy for kidney stones: a review of cellulose sodium phosphate, acetohydroxamic acid, and potassium citrate. 389 14

Potassium citrate (10 mM, pH 6) inhibits the growth of cultured (Glycine max L.) cells when urea is the sole nitrogen source. Ureadependent citrate toxicity is overcome by three separate additions to the growth medium: (a) NH(4)Cl (20 mM); (b) high levels of MgCl(2) (10 mM) or CaCl(2) (5-10 mM); (c) low levels of NiSO(4) (10(-2) mM). Additions of 10(-2) mM NiSO(4) not only overcome citrate growth inhibition but the resultant growth is usually better than urea-supported growth in basal medium (neither added citrate nor added nickel). In the absence of added citrate, exceedingly low levels of NiSO(4) (10(-4) mM) strongly stimulate urea-supported growth in suspension cultures.Citrate does not inhibit growth when arginine is sole nitrogen source. However, cells using arginine have no net urease synthesis in the presence of 10 mM potassium citrate. When 10(-2) mM NiSO(4) is added to this medium, urease specific activity is 10 times that observed in basal medium lacking both citrate and added nickel.Citrate is a chelator of divalent cations. That additional Mg(2+) or Ca(2+) alleviates urea-dependent citrate toxicity indicates that citrate is acting by chelation, probably of another trace divalent cation; this is probably Ni(2+) since at 10(-2) mM it overcomes citrate toxicity and at 10(-4) mM it stimulates urea-supported growth in the absence of citrate. That ammonia overcomes citrate toxicity indicates that the trace Ni(2+) is essential specifically for the conversion of urea to ammonia. Ni(2+) stimulation of urease levels in arginine-grown cells supports this contention.In basal medium, soybean cells grow slowly with urea nitrogen source presumably because the trace amounts of Ni(2+) present (</=10(-6) mM) are growth-limiting.
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PMID:Nitrogen Metabolism in Soybean Tissue Culture: II. Urea Utilization and Urease Synthesis Require Ni. 1665 50