A colorimetric 96-well microtiter plate assay for the determination of urate oxidase activity and its kinetic parameters

Fraisse, Laurent; Bonnet, Marie-Laure; Farcy, Jacques Philippe de; Agut, Christophe; Dersigny, Didier; Bayol, Alain

doi:10.1016/s0003-2697(02)00293-2

Cited by 56 publications

(33 citation statements)

References 21 publications

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“…By contrast, urate, a strong peroxynitrite scavenger, had no effect on cryptogein-mediated cell death. Because urate may be oxidized to allantoin and H 2 O 2 by urate oxidases (Fraisse et al, 2002), and consequently may induce changes to the redox state of the cells, we also investigated the effect of MnTBAP, a permeable superoxide dismutase mimetic, also acting as a peroxynitrite scavenger (Malan et al, 2003). Like urate, MnTBAP did not reduce cryptogein-induced cell death.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Nitric Oxide Signaling Functions in Tobacco Cells Challenged by the Elicitor Cryptogein

et al. 2004

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Nitric oxide (NO) has recently emerged as an important cellular mediator in plant defense responses. However, elucidation of the biochemical mechanisms by which NO participates in this signaling pathway is still in its infancy. We previously demonstrated that cryptogein, an elicitor of tobacco defense responses, triggers a NO burst within minutes in epidermal sections from tobacco leaves (Nicotiana tabacum cv Xanthi). Here, we investigate the signaling events that mediate NO production, and analyze NO signaling activities in the cryptogein transduction pathway. Using flow cytometry and spectrofluorometry, we observed that cryptogein-induced NO production in tobacco cell suspensions is sensitive to nitric oxide synthase inhibitors and may be catalyzed by variant P, a recently identified pathogen-inducible plant nitric oxide synthase. NO Moreover, NO appears to be involved in the pathway(s) leading to the accumulation of transcripts encoding the heat shock protein TLHS-1, the ethyleneforming enzyme cEFE-26, and cell death. In contrast, NO does not act upstream of the elicitor-induced activation of mitogenactivated protein kinase, the opening of anion channels, nor expression of GST, LOX-1, PAL, and PR-3 genes. Collectively, our data indicate that NO is intimately involved in the signal transduction processes leading to cryptogein-induced defense responses.Plants are frequently challenged by potential pathogens and have therefore evolved inducible defense mechanisms to survive in their environment. The activation of plant defense responses is initiated through the recognition of microorganism-derived molecules called elicitors, which trigger rapid defense responses via complex signal transduction pathways (Scheel, 1998). Plant defense responses classically include the production of active oxygen species (AOS), reinforcement of cell walls, and enhanced expression of a large number of defense-related genes, including those encoding cell wall proteins, enzymes involved in the phenylpropanoid biosynthetic pathway, and pathogenesis-related (PR) proteins (Fritig et al., 1998). Plants resisting pathogen attack sometimes develop a hypersensitive response (HR) in which rapid, localized cell death is associated with the restriction of invaders to the infection site (Lam et al., 2001). The HR shares some features of the apoptotic cell death process in animals, and it may likewise represent a type of programmed cell death (PCD; Lam et al., 2001). Moreover, plants usually develop a long-lasting resistance to diverse pathogens via systemic acquired resistance (SAR) or the less well understood induced systemic resistance (ISR; Pieterse et al., 1998).Cryptogein is a basic 10-kD proteinaceous elicitor secreted by the hemibiotrophic oomycete Phytophthora cryptogea (Ricci, 1997). The application of nanomolar concentrations of cryptogein to tobacco plants triggers expression of defense-related genes, induces an HR-like response, and inaugurates the protection of plants against invasion by a broad spectrum of microorganisms including...

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Section: Discussionmentioning

confidence: 99%

Analysis of Nitric Oxide Signaling Functions in Tobacco Cells Challenged by the Elicitor Cryptogein

et al. 2004

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“…Since it is not secreted or reabsorbed by the kidneys, we hypothesized that the allantoin urinary level might be a suitable biological indicator of uric acid catabolism under rasburicase treatment. Currently available techniques are based on colorimetry [5], Clinical Biochemistry 39 (2006) 86 -90 reversed-phase high performance liquid chromatography (HPLC) [6][7][8][9][10][11][12][13], HPLC with precolumn derivation [14], gas chromatography [15], and mass spectrometry [16]. They all require fastidious sample preparation and prolonged analysis time (often up to 24 h).…”

Section: Introductionmentioning

confidence: 99%

Quantification of urinary allantoin by capillary zone electrophoresis during recombinant urate oxydase (rasburicase) therapy

Kattygnarath¹,

Mounier

Madelaine-Chambrin

et al. 2006

Clinical Biochemistry

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“…Previous studies on rasburicase pharmacokinetics were performed by employing an immunometric method based on rather expensive specific antibodies against urate oxidase [22]. Such a method enabled the determination of the enzyme content in serum samples, but gave no information as to the real activity of the enzyme, which therefore is assumed to be proportional to its concentration.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and (Pharmaco)Kinetics of One Single Dose of Rasburicase in Patients with Chronic Kidney Disease

Sestigiani¹,

Mandreoli²,

Guardigli

et al. 2008

Nephron Clin Pract

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Aims: Hyperuricemia is a risk factor associated with cardiovascular and renal disease. Recently, rasburicase, a recombinant urate oxidase, has been developed for the treatment of hyperuricemia in patients with primarily hematological malignancies. We studied the pharmacokinetics and metabolism of rasburicase in the treatment of chronic asymptomatic hyperuricemia in chronic kidney disease (CKD) patients. Materials and Methods: We studied 9 CKD patients with hyperuricemia, whose mean serum acid concentration was 10.2 (range 8.3–15.8) mg/dl. No study subject was taking allopurinol (3/9 are allopurinol intolerant). Patients were treated with rasburicase (0.2 mg/kg/day) in single dose by intravenous infusion over a 30-min period. Serum samples were collected after 1, 4, 8, 24, 48 and 72 h, after 1 week, and after 1 month. To evaluate the efficacy of rasburicase, plasma and urinary concentrations of uric acid were determined by the standard method; the plasma activity of rasburicase was determined using a new assay developed by our laboratory (chromatography-mass method, a colorimetric 96-well microtiter plate assay). Results: All the treated patients experienced a rapid reduction in their plasma uric acid concentration. Data showed an undetectable value within 1 h of treatment. The rasburicase effect ended after 50 h, with a slow increase in the plasma level of uric acid. Conclusion: A single dose of rasburicase is highly effective and well tolerated in the treatment of hyperuricemia in selected CKD patients.

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A colorimetric 96-well microtiter plate assay for the determination of urate oxidase activity and its kinetic parameters

Cited by 56 publications

References 21 publications

Analysis of Nitric Oxide Signaling Functions in Tobacco Cells Challenged by the Elicitor Cryptogein

Analysis of Nitric Oxide Signaling Functions in Tobacco Cells Challenged by the Elicitor Cryptogein

Quantification of urinary allantoin by capillary zone electrophoresis during recombinant urate oxydase (rasburicase) therapy

Efficacy and (Pharmaco)Kinetics of One Single Dose of Rasburicase in Patients with Chronic Kidney Disease

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