Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Free radical attack upon uric acid (UA) nonenzymatically generates allantoin (ALT), and the presence of ALT in human plasma suggests free radical intervention within the body. To assess this possibility, we determined plasma ALT in patients with chronic renal failure (CRF) and some other diseases by high-performance liquid-chromatography (HPLC). Heparinized blood samples were obtained from 15 healthy controls, CRF patients under conservative management (n = 13) or hemodialysis (HD) treatment (n = 8) and patients with gout (n = 11) or rheumatoid arthritis (RA, n = 13). Although not seen in normal plasma samples, ALT was detected in 63% and 31% of patients receiving HD and conservative treatment, respectively. The plasma ALT level decreased after each HD session. ALT was also detected in 18% and 23% of the patients with gout and RA, respectively. ALT was found to be generated by ultraviolet radiation or by the addition of H2O2 to a normal pool-plasma. Addition of Fe(2+) and H2O2 increased the ALT level to about twice that of only H2O2. Addition of either catalase, desferal, EDTA, DMTU, DMSO or mannitol to the plasma decreased ALT generation. These findings suggest that ALT is generated from UA attacked by free radicals, especially by the hydroxyl radical, and that UA plays a role as an antioxidant in the plasma of patients with CRF and some other diseases.
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PMID:[A new role of uric acid as an antioxidant in human plasma]. 260 55

A method is presented to study the effect of drugs on membrane permeability. It is based on the reduction of a spin label trapped in the internal aqueous compartment(s) of membranes by ascorbate ions added to the bulk aqueous phase. The decay of the electron spin resonance signal of the spin label as a function of time gives an indication of the effect of added agents on the permeability of membranes. To demonstrate the technique, the effect on model membranes of egg phosphatidylcholine of the gout-implicated compound monosodium urate, the aprotic solvent dimethyl sulfoxide and the polyene antibiotic amphotericin B were examined. Monosodium urate did not affect the permeability, casting doubt on a proposed mechanism whereby the agent disrupts the membranes via hydrogen bonding. Dimethyl sulfoxide promoted a gradual increase in rate of solute passage across cholesterol-containing model membranes. Amphotericin B had a pronounced effect on the permeability of cholesterol-containing membranes, causing nearly total loss of paramagnetism immediately after addition. Some aspects of the mechanism of action of the drugs are discussed as well as the advantages and disadvantages of the method. The experiments also allow the evaluation of the effect of surface charge and cholesterol on the dimensions of model membranes.
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PMID:Spin label reduction kinetics, a procedure to study the effect of drugs on membrane permeability: the effects of monosodium urate, dimethyl sulfoxide and amphotericin B. 626 83