Disposable luminol copolymer-based biosensor for uric acid in urine.

A new electrochemiluminescent (ECL) disposable biosensor for uric acid was manufactured by immobilization in a double-layer design of luminol as a copolymer with 3,3',5,5'-tetramethylbenzidine (TMB) and the enzyme uricase in chitosan on gold screen-printed cells. The good mechanical and improved electroluminescent characteristics of the new copolymer poly(luminol-TMB) make it possible to determine uric acid by measuring the growing ECL emission with the analyte concentration. The combination of enzymatic selectivity with ECL sensitivity results in a disposable analytical device with a linear range for uric acid from 1.5×10(-6) to 1.0×10(-4) M, a limit of detection of 4.4×10(-7) M and a precision of 13.1% (1.0×10(-5) M, n=10) as relative standard deviation. Satisfactory results were obtained for uric acid determination in 24h-urine samples compared to a reference procedure. This uric acid biosensor can be used as a low-cost alternative to conventional methods.

Low-potential detection of endogenous and physiological uric acid at uricase-thionine-single-walled carbon nanotube modified electrodes.

This work develops and validates an electrochemical approach for uric acid (UA) determinations in both endogenous (cell lysate) and physiological (serum) samples. This approach is based on the electrocatalytic reduction of enzymatically generated H(2)O(2) at the biosensor of uricase-thionine-single-walled carbon nanotube/glassy carbon (UOx-Th-SWNTs/GC) with the use of Th-SWNTs nanostructure as a mediator and an enzyme immobilization matrix. The biosensor, which was fabricated by immobilizing UOx on the surface of Th-SWNTs, exhibited a rapid response (ca. 2 s), a low detection limit (0.5 +/- 0.05 microM), a wide linear range (2 microM to 2 mM), high sensitivity (approximately 90 microA mM(-1) cm(-2)), as well as good stability and repeatability. In addition, the common interfering species, such as ascorbic acid, 3,4-dihydroxyphenylacetic acid, 4-acetamidophenol, etc., did not cause any interference due to the use of a low operating potential (-400 mV vs saturated calomel electrode). Therefore, this work has demonstrated a simple and effective sensing platform for selective detection of UA in the physiological levels. In particular, the developed approach could be very important and useful to determine the relative role of endogenous and physiological UA in various conditions such as hypertension and cardiovascular disease.

Management of hyperuricemia with rasburicase review.

Tumor lysis syndrome (TLS) is a serious complication in patients with hematological malignancies. Massive lysis of tumor cells can lead to hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcaemia. These metabolic disturbances may result in renal failure, because of precipitation of uric acid crystals and calcium phosphate salts in the kidney. The standard prophylaxis or treatment of hyperuricemia consists of decreasing uric acid production with allopurinol and facilitating its excretion by urinary alkalinization and hyperhydration. By inhibiting the enzyme xanthine oxidase, allopurinol blocks the conversion of hypoxanthine and xanthine into uric acid. An alternative treatment is urate oxidase which oxidates uric acid into allantoin. Allantoin is 5-10 times more soluble than uric acid and is therefore excreted easily. In several clinical trials rasburicase, the recombinant form of urate oxidase, has shown to be very effective in preventing and treating hyperuricemia. Rasburicase, in contrast with the non-recombinant form of urate oxidase uricozyme, is associated with a low incidence of hypersensitivity reactions. In addition to the demonstrated clinical benefit, rasburicase also proved to be a cost-effective option in the management of hyperuricemia.