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PubMed2006

Photodegradation of orange I in the heterogeneous iron oxide-oxalate complex system under UVA irradiation.

To understand the photodegradation of azo dyes in natural aquatic environment, a novel photo-Fenton-like system, the heterogeneous iron oxide-oxalate complex system was set up with the existence of iron oxides and oxalate. Five iron oxides, including gamma-FeOOH, IO-250, IO-320, IO-420 and IO-520, were prepared and their adsorption capacity was investigated in the dark. The results showed that the saturated adsorption amount (gamma(max)) was ranked the order of IO-250 > IO-320 > gamma-FeOOH > IO-420 > IO-520 and the adsorption equilibrium constant (Ka) followed the order of IO-250 > IO-520 > gamma-FeOOH > IO-420 > IO-320. The effect of initial pH value, the initial concentrations of oxalate and orange I on the photodegradation of orange I were also investigated in different iron oxide-oxalate systems. The results showed that the photodegradation of orange I under UVA irradiation could be enhanced greatly in the presence of oxalate. And the optimal oxalate concentrations (C(ox)0) for gamma-FeOOH, IO-250, IO-320, IO-420 and IO-520 were 1.8, 1.6, 3.5, 3.0 and 0.8 mM, respectively. The photodegradation of orange I in the presence of optimal C(ox)0 was ranked as the order of gamma-FeOOH > IO-250 > IO-320 > IO-420 > IO-520. The optimal range of initial pH was at about 3-4. The first-order kinetic constant for the degradation of orange I decreased with the increase in the initial concentration of orange I. Furthermore, the variation of pH, the concentrations of Fe3+ and Fe2+ during the photoreaction were also strongly dependent on the C(ox)0 and iron oxides.

Azo Compounds↗
PubMed2004

Armepavine oxalate induces cell death on CCRF-CEM leukemia cell line through an apoptotic pathway.

Drug-induced cell death can occur as a result of DNA damage, which in turn may lead to the reduction of bcl-2 expression and activation of caspase-3 expression. In the present study, we investigated the effect of armepavines and atherosperminine on the cell survival rate and expression of bcl-2 and caspase-3 in CCRF-CEM cells. Our data have revealed that armepavine oxalate reduced the survival rate of CCRF-CEM cells in a dose- and time-dependent manner by MTT assay. However, no significant effects of armepavine MeI and atherosperminine N-oxide on the survival rate of the CCRF-CEM cell were observed. Armepavine oxalate-induced cell death was considered to be apoptotic on the basis of observed formation of the DNA ladder and the typical apoptotic morphological change by Hoechst 33258 staining. The expression of bcl-2 protein in CCRF-CEM cells treated with 30 microM armepavine oxalate was significantly decreased in western blotting analysis. In contrast, the expression of active caspase-3 in the cells was increased by armepavine oxalate in a dose-dependent manner. These findings indicate the involvement of bcl-2 and caspase-3 in the apoptotic process of CCRF-CEM cells induced by armepavine oxalate. The increased expression of active caspase-3 as well as decreased expression of bcl-2 support the assumption the armepavine oxalate-treated cells may be capable to complete the entire apoptotic process ending in cell fragmentation.

Alkaloids↗
PubMed2006

Renal peroxidative changes mediated by oxalate: the protective role of fucoidan.

Oxalate, one of the major constituents of renal stones is known to induce free radicals which damage the renal membrane. Damaged epithelia might act as nidi for stone formation aggravating calcium oxalate precipitation during hyperoxaluria. In the present study, the beneficial effects of fucoidan on oxalate-induced free radical injury were investigated. Male Wistar rats were divided into four groups. Hyperoxaluria was induced in two groups by administration of 0.75% ethylene glycol in drinking water for 28 days and one of them was treated with fucoidan from Fucus vesiculosus at a dose of 5 mg/kg b.wt subcutaneously commencing from the 8th day of induction. A control and drug control (fucoidan alone) was also included in the study. The extent of renal injury in hyperoxaluria was evident from the increased activities of alkaline phosphatase, gamma-glutamyl transferase, beta-glucuronidase, N-acetyl-beta-D-glucosaminidase in urine. There was a positive correlation between plasma malondialdehyde levels and renal membrane damage indicating a striking relation between free radical formation and cellular injury. Increased protein carbonyl and decreased thiols further exemplified the oxidative milieu prevailing during hyperoxaluria. Decreased renal membrane ATPases accentuated the renal membrane damage induced by oxalate. Renal microscopic analysis showed abnormal findings in histology as an evidence of oxalate damage. The above biochemical and histopathological discrepancies were abrogated with fucoidan administration, indicating its protective role in oxalate mediated peroxidative injury.

Animals↗
PubMed2001

Diets with either beef or plant proteins reduce risk of calcium oxalate precipitation in patients with a history of calcium kidney stones.

OBJECTIVE: To determine the effect of substituting equal amounts of dietary protein as animal protein (beef) for plant protein (legumes, seeds, nuts, and grains) on urinary components associated with calcium oxalate precipitability risk. DESIGN: Randomized crossover trial. SUBJECTS: Twenty-three normocalciuric patients with a history of calcium kidney stones (8 women and 15 men, mean age 50.7+/-14.6 years) with 24-hour urinary calcium < or =10.3 micromol, 24 hour urinary oxalate excretion between 228 and 963 micromol, and a urinary calcium increase of < or =1.0 micromol in 4 hours after a 25 micromol oral calcium load. SETTING: Four-day, free-living adaptation period, followed by 2-day metabolic unit study. INTERVENTION: The study compared consumption of 2 servings of beef (43 g protein for women and 50 g for men) daily with an equal amount of protein from plant foods including legumes, nuts, and grains. MAIN OUTCOME MEASURES: Tiselius risk index (TRI) for calcium oxalate precipitability calculated from urinary calcium, oxalate, magnesium, citrate, and volume. STATISTICAL ANALYSES: Paired t tests. RESULTS: Urinary calcium, oxalate, magnesium, citrate, phosphorus, volume, and TRI did not differ between diets. Urinary sodium and potassium were higher for patients on the plant protein diet. After correcting for variations in urinary sodium and potassium between diets, the difference in urinary calcium remained insignificant. TRI was lower on both beef- and plant-protein diets compared with self-selected prestudy diets for all participants. CONCLUSION/APPLICATIONS: Balanced diets containing moderate amounts of either beef or plant protein are equally effective in reducing calcium oxalate kidney stone risk based on changes in urinary composition.

Adult↗
PubMed1998

Quantitative determination of oxalate and other organic acids in drinking water at low microgram/1 concentrations.

In this research, a recently developed ion chromatography method for organic acids was expanded to include oxalate. A major challenge was that oxalate elutes between inorganic anions such as sulfate, phosphate, bromide and nitrate, which are often present in much higher concentrations than oxalate. Optimization of the previously reported method made it possible to determine oxalate in these matrices. However, for those samples in which higher inorganic anion concentrations caused the oxalate peak to be obscured, a "heart-cut" column switching technique was used as an alternative. The method detection limit for oxalate was 9 micrograms/l with the direct approach and 6 micrograms/l for the "heat-cut" technique. These modifications represent a valuable supplement to a recently developed method for monitoring ozonation by-products in drinking water.

Anions↗
PubMed1998

The effect of (L)-cysteine and (L)-2-oxothiazolidine-4-carboxylic acid (OTZ) on urinary oxalate excretion: studies using a hyperoxaluric rat model.

PURPOSE: To determine the efficacy of (L)-cysteine and (L)-2-oxothiazolidine-4-carboxylic acid (OTZ) in reducing urinary oxalate excretion under hyperoxaluric conditions and to determine whether by inclusion of glycolate in a standard diet, cysteine:glyoxylate adduct can be detected in hyperoxaluric rats given either compound. MATERIALS AND METHODS: Hyperoxaluria (200% above basal) was induced 2 days prior to commencement of the studies and maintained throughout. After a 3 days baseline, animals were randomly allocated to a control or treatment group. Standard diet containing either (L)-cysteine or OTZ was then fed to the treatment groups for 5 days while standard diet alone was fed to the control groups. Urinary oxalate excretion was subsequently monitored and average daily rates were then compared with basal values. Plasma and urine were analyzed for adduct. RESULTS: Both (L)-cysteine and OTZ significantly reduced urinary oxalate excretion relative to the basal hyperoxaluric level (28.6 +/- 1.5 micromol./day). While (L)-cysteine reduced oxalate excretion over the 5 day treatment period by only 7.82 +/- 1.39 micromol./day (27%), OTZ reduced it by 12.34 +/- 1.58 micromol./day (43%). Adduct could not be detected in plasma or urine in this study. CONCLUSIONS: This study confirms that both (L)-cysteine and OTZ are effective in reducing urinary oxalate excretion under hyperoxaluric conditions, with OTZ being more effective than (L)-cysteine. These compounds were shown to be 3- to 4-fold more effective in reducing urinary oxalate excretion under hyperoxaluric conditions when compared with the results from previous studies under normooxaluric conditions.

Animals↗
PubMed1994

Oxalate transport in a line of porcine renal epithelial cells--LLC-PK1 cells.

The present studies examined oxalate handling in LLC-PK1 cells, an epithelial cell line of porcine origin. These cells appear to express transport systems for oxalate, as evidenced by the fact that uptake was saturable, time dependent and sensitive to the anion transport inhibitor DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid). Oxalate uptake in these cells was also affected by the presence of certain inorganic anions (Cl-, SO4(2-), or HCO3-) but not by organic anions (para-aminohippurate, urate, malate, phenylsuccinate, succinate). This uptake was Na independent and unaffected by changes in membrane potential but was affected by external pH, with acidic pH stimulating and alkaline pH inhibiting oxalate accumulation. These findings suggest that LLC-PK1 cells express oxalate transporters similar to those observed in the mammalian renal cortex. Further studies using these cells may prove useful in defining the conditions that govern transcellular oxalate flux in renal epithelial cells.

Animals↗
PubMed1980

Renal oxalate excretion in calcium urolithiasis.

Urinary oxalate was determined in an ambulatory setting in 107 patients with an increased intestinal calcium absorption rate in whom stones formed, 34 patients with normal calcium absorption in whom stones formed and 34 control subjects without stones. Urinary oxalate excretion was not significantly different when the diet was changed from a random to a calcium-restricted diet. Moreover, urinary oxalate was not higher during summer months when intestinal calcium absorption may have been stimulated. Diet history disclosed that many patients with an increased calcium absorption rate had been on a moderate oxalate-restricted diet, often as part of a calcium-restricted regimen for the control of hypercalciuria. The results indicate that renal oxalate excretion in an ambulatory setting is not critically dependent on the state of calcium absorption and intake, and that the imposition of a low calcium dietary regimen in patients with an increased calcium absorption and in whom stones form does not necessarily augment oxalate excretion.

Adult↗
PubMed1992

Effects of ascorbic acid and pyridoxine supplementation on oxalate metabolism in peritoneal dialysis patients.

We studied the effect of vitamin C and B6 supplementation on oxalate metabolism in seven patients receiving chronic peritoneal dialysis therapy. The study was divided into three phases, each lasting 4 weeks. Plasma oxalate, total ascorbic acid, and pyridoxal-5'-phosphate (PLP) were measured at the end of each phase. Twenty-four-hour urinary excretion and dialysate removal rates of oxalate were also obtained. At the end of phase I (supplement-free period), plasma oxalate levels were markedly elevated at 47.6 +/- 7.1 mumol/L (437 +/- 66 micrograms/dL) (normal, 3.4 +/- 0.4 mumol/L [30.3 +/- 1.6 micrograms/dL]). Plasma total ascorbic acid levels were 62 +/- 6 mumol/L (1.0 +/- 0.1 mg/dL) (normal, 45 to 57 mumol/L [0.8 to 1.0 mg/dL]), while plasma PLP levels were markedly reduced to 24 +/- 5 nmol/L (normal, 40 to 80 nmol/L). Daily supplements of 0.57 mmol (100 mg) ascorbic acid orally (phase II) resulted in a 19% increase in the plasma oxalate levels to 57.8 +/- 6.1 mumol/L (520 +/- 55 micrograms/dL) (P less than 0.03), with a concomitant 60% increase in the plasma ascorbate levels (91 +/- 6 mumol/L [1.6 +/- 0.1 mg/dL], P less than 0.01). Plasma PLP values remained low. Finally, during phase III (0.57 mmol or 100 mg ascorbic acid plus 59.6 mumol or 10 mg pyridoxine HCI orally daily), plasma oxalate levels declined by 17% to 47.9 +/- 5.2 mumol/L (431 +/- 47 micrograms/dL) (P greater than 0.05 v phase II).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Cloning and expression of the oxalyl-CoA decarboxylase gene from the bacterium, Oxalobacter formigenes: prospects for gene therapy to control Ca-oxalate kidney stone formation.

Evidence suggests that the formation of calcium-oxalate stones in the urine is dependent on the saturation levels of both calcium and oxalate; thus, management of one or both of these ions in individuals susceptible to urolithiasis appears important. Since there are no known naturally occurring enzymes in vertebrates capable of degrading oxalate, we have initiated a study to insert a plant-derived oxalate degrading enzyme gene into human cells as a means of lowering plasma and urinary oxalate concentrations. We present here the cloning of the oxalyl-CoA decarboxylase gene from the bacterium Oxalobacter formigenes and its subsequent expression in a foreign environment. These results provide the basis for eventual transfer of an oxalate decarboxylase gene into mammalian cells.

Bacteria, Anaerobic↗
PubMed2002

Risk of calcium oxalate nephrolithiasis in postmenopausal women supplemented with calcium or combined calcium and estrogen.

BACKGROUND: Recent studies showed that postmenopausal women lost less bone mass when supplemented with calcium or estrogen therapy. However, the safety of the treatments in terms of the risk of calcium oxalate stone formation is unknown. We therefore conducted this study to determine the alteration in calcium oxalate supersaturation after calcium supplement or after combined calcium and estrogen therapy in postmenopausal osteoporotic women. METHODS: Fifty-six postmenopausal women were enrolled in this study. All subjects were more than 10 years postmenopausal with vertebral or femoral osteoporosis by bone mineral density criteria. They were randomly allocated to receive either 625 mg of calcium carbonate (250 mg of elemental calcium) at the end of a meal three times a day (group A, n=26) or calcium carbonate in the same manner plus 0.625 mg/day of conjugated equine estrogen and 5 mg medrogestone acetate from day 1-12 each month (group B, n=30). The age (mean +/- S.E.M.) was 66.3 +/- 1.2 and 65.1 +/- 1.1 years, weight 54.1 +/- 1.2 and 55.3 +/- 2.1 kg, in group A and group B, respectively. Urine specimens (24-h) were collected at baseline and 3 months after treatment for the determination of calcium oxalate saturation by using Tiselius's index (AP(CaOx)) and calcium/citrate ratio. RESULTS: After 3 months of treatment, there was no significant alteration from baseline for urinary excretion of calcium, citrate and oxalate. Urinary phosphate excretion was significantly reduced (6.3 +/- 0.7 vs. 5.1 +/- 0.7 mmol/day for group A and 8.2 +/- 0.9 vs. 5.8 +/- 0.7 mmol/day for group B, P<0.05), whereas net alkaline absorption was significantly elevated (10.1 +/- 3.6 vs. 20.1 +/- 4.4 meq/day for group A and 4.8 +/- 3.2 vs. 19.9 +/- 3.6 meq/day for group B, P<0.05). Calcium/citrate ratio and AP(CaOx) determined at baseline were not different from the corresponding values after treatment in both groups; calcium/citrate: 10.1 +/- 3.1 vs. 10.1 +/- 2.5 for group A and 9.3 +/- 1.8 vs. 11.9 +/- 2.5 for group B and AP(CaOx): 1.1 +/- 0.1 vs. 1.3 +/- 0.2 for group A and 1.2 +/- 0.2 vs. 1.1 +/- 0.1 for group B. There were eight and nine patients with high AP(CaOx), or >2, at baseline and after treatment, respectively. CONCLUSIONS: Calcium supplement with a meal or combined calcium supplement and estrogen therapy is not associated with a significant increased risk of calcium oxalate stone formation in the majority of postmenopausal osteoporotic patients. Determination of urinary saturation for calcium oxalate after calcium and estrogen supplements, especially at the initial phase of treatment, may be helpful in the avoidance of nephrolithiasis.

Aged↗
PubMed1988

Coordination of manganous ion at the active site of pyruvate, phosphate dikinase: the complex of oxalate with the phosphorylated enzyme.

Electron paramagnetic resonance spectroscopy has been used to investigate the structure of the complex of manganous ion with the phosphorylated form of pyruvate,phosphate dikinase (Ep) and the inhibitor oxalate. Oxalate, an analogue of the enolate of pyruvate, is competitive with respect to pyruvate in binding to the phosphorylated form of the enzyme [Michaels, G., Milner, Y., & Reed, G.H. (1975) Biochemistry 14, 3213-3219]. Superhyperfine coupling between the unpaired electrons of Mn(II) and ligands specifically labeled with 17O has been used to identify oxygen ligands to Mn(II) in the complex with oxalate and the phosphorylated form of the enzyme. Oxalate binds at the active site as a bidentate chelate with Mn(II). An oxygen from the 3'-N-phosphohistidyl residue of the protein is in the coordination sphere of Mn(II), and at least two water molecules are also bound to Mn(II) in the complex. Oxalate also binds directly to Mn(II) in a complex with nonphosphorylated enzyme. The structure for the Ep-Mn(II)-oxalate complex implies that simultaneous coordination of a phospho group and of the attacking nucleophile to the divalent cation is likely an important factor in catalysis of this phospho-transfer reaction.

Binding Sites↗
PubMed2001

Increased Septoria musiva resistance in transgenic hybrid poplar leaves expressing a wheat oxalate oxidase gene.

A cDNA clone of a wheat germin-like oxalate oxidase (OxO) gene regulated by the constitutive CaMV 35S promoter was expressed in a hybrid poplar clone, Populus x euramericana ('Ogy'). Previous studies showed that OxO is likely to play an important role in several aspects of plant development, stress response, and defense against pathogens. In order to study this wheat oxalate oxidase gene in woody plants, the expression of this gene and the functions of the encoded enzyme were examined in vitro and in vivo in transgenic 'Ogy'. The enzyme activity in the transformed 'Ogy' was visualized by histochemical assays and in SDS-polyacrylamide gels. It was found that the wheat OxO gene is expressed in leaves, stems, and roots of the transgenic 'Ogy' plants and the encoded enzyme is able to break down oxalic acid. Transgenic 'Ogy' leaves were more tolerant to oxalic acid as well as more effective in increasing the pH in an oxalic acid solution when compared to untransformed controls. In addition, when leaf disks from 'Ogy' plants were inoculated with conidia of the poplar pathogenic fungus Septoria musiva, which produces oxalic acid, the OxO-transformed plants were more resistant than the untransformed controls.

Ascomycota↗
PubMed1979

Oxalate excretion in rats injected with xylitol or glycollate: stimulation by phenobarbitone pre-treatment.

The hypothesis that the prior intake of barbiturates may predispose patients to form increased amounts of oxalate following the intravenous infusion of xylitol was investigated in the rat. Phenobarbitone pre-treatment resulted in a 2-3 fold increase in urinary [14C] oxalate concentration following the intraperitoneal injection of [U-14C] xylitol or [l -14C] glycollate. The absence of any marked changes in urine volumes and creatinine excretion implied that this increase in urinary oxalate excretion was due to the enhanced synthesis of oxalate. The activities of key enzymes in hepatic oxalate synthesis, glycollate oxidase, lactate dehydrogenase, catalase and alanine aminotransferase were not altered by phenobarbitone pre-treatment. It is suggested that the increased activity of the microsomal mixed function oxidases, following phenobarbitone treatment, may facilitate the oxidation of glycollate and possibly xylitol. This communication leads experimental support to the concept that the prior intake of drugs, such as barbiturates, may predispose patients to form increased amounts of oxalate.

Animals↗
PubMed1979

Effect of para-aminohippurate on renal transport of oxalate.

Infusion of para-aminohippurate (PAH) at rates below the maximum rate of transport (Tm) of PAH in the rat resulted in a significant decrease in the fractional excretion of oxalate (FEox) from 128.1% to 113.9% (P less than 0.01). Fractional delivery of oxalate (FDox) to the early proximal tubule, however, was unchanged from control values, whereas FDox to the late proximal tubule was significantly decreased from 126.4% to 107.4% (P less than 0.01). Infusion of PAH at rates above Tm of PAH resulted in a decrease in FDox to the early proximal tubule to 105.3% and to the late proximal tubule to 105.5%, and in FEox to 100.5%. These changes were not the result of alterations in urinary sodium or bicarbonate excretion. Microinjection studies indicated that PAH did not affect the tubular absorption of oxalate. These studies suggest that PAH inhibits the tubular secretion of oxalate and that there may be more than one secretory system for oxalate with differing affinities for oxalate and PAH in the early and late proximal tubules.

Aminohippuric Acids↗
PubMed1985

Bladder secretion of inhibitors of calcium oxalate crystal growth.

Differences in calcium oxalate crystal growth inhibition were studied in normally voided urine (bladder urine) and in urine collected directly from the kidney (kidney urine) in nine dogs. Urine samples were collected before and 10 days after bilateral ureterostomies. Calcium oxalate crystal growth inhibition was measured in a standard seeded crystal growth system. The alcian blue-precipitable material of the urine samples was determined. Significantly lower values were observed in kidney urine than in bladder urine for calcium oxalate crystal inhibition (mean difference, 0.07 +/- 0.02 inhibitor units/mg creatinine; P less than 0.01) and for the alcian blue-precipitable material (mean difference, 0.07 +/- 0.02 mg/mg creatinine; P less than 0.01). We conclude that the bladder adds calcium oxalate crystal growth inhibition to urine. Glycosaminoglycans from the bladder mucosa may be responsible; however, other acidic polymers such as RNA fragments or glycopeptides have been shown to be a constituent of the alcian blue-precipitable material. These are potent inhibitors of calcium oxalate crystal growth, and their participation in the increase of inhibition observed in bladder urine cannot be excluded. Total calcium oxalate crystal growth inhibition present in normally voided urine may be an overestimation of the actual inhibition present at the level of the kidney, where calculi usually form.

Alcian Blue↗
PubMed1992

Calcium oxalate crystallization in urine: role of urate and glycosaminoglycans.

Increasing the concentration of urate promotes the crystallization of calcium oxalate in human urine. In this study the possibility that this effect might be attributable to the attenuation of the inhibitory activity of urinary glycosaminoglycans (GAGs) was explored. Urine sample were collected from 20 men with no history of urolithiasis and the intact GAGs removed by 10 kDa ultrafiltration. Ten of these specimens, designated type A, spontaneously precipitated calcium oxalate crystals when the median urate concentration was increased from 3.13 to 7.33 mmol/liter by the addition of a saturated solution of sodium urate. In the remaining more dilute urines, which were designated type B, spontaneous calcium oxalate crystallization did not occur when the median urate concentration was raised from 2.20 to 6.40 mmol/liter. In these samples crystallization was induced by a standard load of oxalate above the empirically determined metastable limit. Addition of urate significantly reduced the median metastable limit from the control value of 125 to 46 mumol oxalate, and the volume of calcium oxalate deposited was increased fourfold from 25,000 to 104,000 microns 3/microliters. The median size of the precipitated particles was also increased in the presence of urate from 12.06 microns to 14.3 microns; this was confirmed by scanning electron microscopy, which demonstrated that the crystals precipitated in the presence of added urate, though individually smaller, were markedly more numerous and more highly aggregated than those deposited in the control. Re-ultrafiltration of the urines to which urate had been added did not alter the urate concentration, and SEM examination of the ultrafiltration membranes did not reveal the presence of any particulate material.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Selective membranes for the construction and optimization of an amperometric oxalate enzyme electrode.

Oxalate oxidase has been immobilized within a membrane laminate. Integration of the laminate within an amperometric electrode afforded a sensor for determining oxalate via electrochemical oxidation of H2O2 and subsequent current generation. A study of novel poly(vinyl chloride) (PVC) and cellulose acetate (CA) membranes with various outer/inner membrane configurations made it possible to eliminate direct electrochemical interference from species present in urine, typically ascorbate (60-500 mumol l-1), homovanillic acid (40-60 mumol l-1) and oxalate itself (50-500 mumol l-1). Of the membranes studied, only CA and plasticized PVC were found to screen out the direct oxalate electrochemical signal effectively. Cellulose acetate exhibited the best selectivity ratio for H2O2 over urine interference. An outer 0.05 micron pore radius polycarbonate membrane imparted sensor linearity in the narrow range 2-200 mumol l-1 oxalate, which fell below the normal range of oxalate in urine. The application of unplasticized PVC as an outer membrane allowed the sensor to exhibit linear characteristics which extended beyond the clinically relevant range (> 700 mumol l-1). The Michaelis-Menten constant of the immobilized enzyme was measured and found to be 10(-3) mol l-1.

Biosensing Techniques↗