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PubMed1985

Calcium oxalate and calcium phosphate capacities of cardiac sarcoplasmic reticulum.

Both oxalate-supported and phosphate-supported calcium uptake by canine cardiac sarcoplasmic reticulum initially increase linearly with time but fall to a steady-state level within 20 min. The departure from linearity could be due to a decrease in influx or to an increase in efflux of calcium. Because Ca2+-ATPase activity is linear, a decrease in the influx of calcium is an unlikely cause of the non-linear calcium uptake curves. A possible cause of an increase in calcium efflux is rupture of the vesicles. This hypothesis was tested by investigating the amount of calcium which could be released upon addition of 5 mM EGTA. The amount of rapidly releasable calcium was zero until a threshold calcium uptake of about 4-6 mumol calcium oxalate or calcium phosphate per mg was reached. After that point the rapidly releasable calcium continued to increase with calcium oxalate to reach more than 23 mumol/mg, but stayed constant at about 0.7 mumol/mg for calcium phosphate. The rapidly releasable calcium was attributed to calcium oxalate or calcium phosphate crystals externalized by vesicle rupture. The differences in the amounts of rapidly releasable calcium were attributed to different kinetics of calcium phosphate and calcium oxalate dissolution. Addition of ryanodine caused a marked increase in the threshold for rapidly releasable calcium oxalate. Transmission electron micrographs showed that vesicles can become filled with calcium oxalate crystals, but the vesicles were heterogeneous with respect to their size and their sensitivity to ryanodine. These observations support the hypothesis that calcium oxalate and calcium phosphate capacities are limited by vesicle rupture and that ryanodine increases the capacity by closing a calcium channel in a subpopulation of vesicles that otherwise would not accumulate calcium.

Adenosine Triphosphate↗
PubMed1984

Oxalate-loading tests to screen for steatorrhoea: an appraisal.

We have evaluated two procedures as screening tests for steatorrhoea: firstly, a simplified, two-day, oxalate-loading test and secondly the rate of urinary oxalate excretion following a single oral dose of oxalate. Following two-day oxalate loading there was almost complete overlap of the values for 24-h urinary oxalate between 15 apparently healthy volunteers and 10 patients with steatorrhoea. The rate of oxalate excretion following a single dose of oxalate was increased in one patient with Crohn's disease and ileal resection who had normal faecal fat excretion, but three patients with steatorrhoea due to other causes had normal rates of excretion. We conclude that these oxalate-loading tests are not a useful alternative to faecal fat estimation in patients with suspected malabsorption.

Adult↗
PubMed1977

The pathways of oxalate formation from phenylalanine, tyrosine, tryptophan and ascorbic acid in the rat.

The metabolic pathway by which L-[14C1]phenylalanine, L-[14C1]tyrosine, L-[14C1]tryptophan, and L-[14C1]ascorbic acid are converted to [14C]oxalate have been investigated in the male rate. Only [14C]oxalate was detected in the urine of rats injected with L-[14C1]ascorbic acid, but [14C]-labeled oxalate, glycolate, glyoxylate, glycolaldehyde, glycine, and serine were recovered from the [14C1]-labeled aromatic amino acids. DL-Phenyllactate, an inhibitor of glycolic acid oxidase and glycolic acid dehydrogenase, reduced the amount of [14C]oxalate recovered in the urine of rats given the [14C1]-labeled aromatic amino acids, but increased the amount of [14C]glycolate formed from L-[14C1]phenylalanine and L-[14C1]tyrosine and the amount of [14C]glycolate produced from [14C1]tryptophan. Based on the [14C]labeled intermediates identified and the relative distribution of the radioactivity, it is postulated that phenylalanine and tyrosine are converted to oxalate via glycolate which is oxidized directly to oxalate by glycolic acid dehydrogenase. Tryptophan is metabolized via glyoxylate which is oxidized directly to oxalate by glycolic acid oxidase. Neither glycolate, glyoxylate, glycolic acid oxidase or glycolic acid dehydrogenase are involved in the formation of oxalate from ascorbic acid.

Animals↗
PubMed1986

Hepatic oxalate production: the role of hydroxypyruvate.

The metabolism of hydroxypyruvate to oxalate was studied in isolated rat hepatocytes. [14C]Oxalate was produced from [2-14C]- and [3-14C]- but not [1-14C]hydroxypyruvate. No oxalate was produced from similarly labeled pyruvate. The mechanism by which hydroxypyruvate is metabolized to oxalate involves decarboxylation at the carbon 1 position as the initial step. This activity was distinct from that which produced CO2 from the carbon 1 position of pyruvate. Hydroxypyruvate decarboxylase activity was found mainly in the mitochondria, with the remainder (25%) in the cytosol. No activity was present in the peroxisomes, the probable site of oxalate production from glycolate and glyoxylate. Hydroxypyruvate, but not pyruvate stimulated [14C]oxalate production from [U-14C]fructose, suggesting that hydroxypyruvate is either an intermediate in the fructose-oxalate pathway, or that it prevents carbon from leaving that pathway. The lack of effect of pyruvate in this regard is evidence against redox being the primary effect of hydroxypyruvate and focuses attention on hydroxypyruvate and its precursors as important sources of carbon for oxalate synthesis from both carbohydrate and protein.

Animals↗
PubMed2005

The effect of oxalic acid incorporation on the setting time and strength of a glass-ionomer cement.

Oxalic acid and its metal oxalate salts have been used extensively in dentistry in a range of applications: as desensitisers, in cavity preparation, and as bonding agents. This study investigated the influence of oxalic acid upon the working time, initial setting time, 24-h hardness and compressive strength of a glass-ionomer cement. Conventional glass-ionomer liquids were prepared from polyacrylic acid, tartaric acid, water, and oxalic acid at concentrations of 0-7% w/w. Liquids were dosed into capsules with a commercial glass-ionomer powder, activated and mixed. The resultant pastes were assessed for working time, initial setting time, 24-h hardness and 24-h compressive strength. Liquids containing 0.5-1% oxalic acid lengthened the working time and initial setting time. At concentrations greater than 2%, both working and initial setting times decreased with increasing oxalic acid. Surface hardness values using liquids with 3% and 7% oxalic acid were less hard than the control. Compressive strength was unchanged over the concentrations tested. Oxalic acid may be a useful reaction modifier in glass-ionomer systems. It accelerated the setting reaction without affecting strength, but was limited to low concentrations because of its relatively poor solubility in water.

Biomechanical Phenomena↗
PubMed2004

The oxalate effect on release of iron from human serum transferrin explained.

A unique feature of the mechanism of iron binding to the transferrin (TF) family is the synergistic relationship between metal binding and anion binding. Little or no iron will bind to the protein without concomitant binding of an anion, physiologically identified as carbonate. Substitution of oxalate for carbonate produces no significant changes in polypeptide folding or domain orientation in the N-lobe of human serum TF (hTF) as revealed by our 1.2A structure. The oxalate is able to bind to the iron in a symmetric bidentate fashion, which, combined with the low pK(a) of the oxalate anion, makes iron displacement more difficult as documented by both iron release kinetic and equilibrium data. Characterization of an N-lobe in which the arginine at position 124 is mutated to alanine reveals that the stabilizing effect of oxalate is even greater in this mutant and nearly cancels the destabilizing effect of the mutation. Importantly, incorporation of oxalate as the synergistic anion appears to completely inhibit removal of iron from recombinant full-length hTF by HeLa S(3) cells, strongly indicating that oxalate also replaces carbonate in the C-lobe to form a stable complex. Kinetic studies confirm this claim. The combination of structural and functional data provides a coherent delineation of the effect of oxalate binding on hTF and rationalizes the results of many previous studies. In the context of iron uptake by cells, substitution of carbonate by oxalate effectively locks the iron into each lobe of hTF, thereby interfering with normal iron metabolism.

Binding Sites↗
PubMed2004

Improving the two-step remediation process for CCA-treated wood: Part I. Evaluating oxalic acid extraction.

In this study, three possible improvements to a remediation process for chromated-copper-arsenate- (CCA) treated wood were evaluated. The process involves two steps: oxalic acid extraction of wood fiber followed by bacterial culture with Bacillus licheniformis CC01. The three potential improvements to the oxalic acid extraction step were (1) reusing oxalic acid for multiple extractions, (2) varying the ratio of oxalic acid to wood, and (3) using a noncommercial source of oxalic acid such as Aspergillus niger, which produces oxalic acid as a metabolic byproduct. Reusing oxalic acid for multiple extractions removed significant amounts of copper, chromium, and arsenic. Increasing the ratio of wood to acid caused a steady decline in metal removal. Aspergillus niger removed moderate amounts of copper, chromium, and arsenic from CCA-treated wood. Although A. niger was effective, culture medium costs are likely to offset any benefits. Repeated extraction with commercial oxalic acid appears to be the most cost-effective method tested for the two-step process.

Arsenates↗
PubMed2005

Iron type catalysts for the ozonation of oxalic acid in water.

Two iron catalysts (Fe(III) and Fe2O3/Al2O3) have been used in the ozonation of oxalic acid in water at pH 2.5. Percentage removals of oxalic acid were 1.8%, 7% and 30% corresponding to the non-catalytic, homogeneous (Fe(III)) and heterogeneous (Fe2O3/Al2O3) catalytic ozonations, respectively. Catalytic oxalic acid ozonation leads in all cases to total mineralization. The mechanism of ozonation likely develops through formation of iron-oxalate complexes that further react with ozone without the participation of hydroxyl radicals. Because of the stringent acidic conditions, some metal leaching has been observed and quantified in the heterogeneous process. In the homogeneous catalysis, the kinetics was found to be first order with respect to ozone and oxalic acid while for the heterogeneous catalysis, the kinetic order depends on the concentration of ozone in the gas fed. Thus, at ozone concentrations lower than 30 mg L(-1), the heterogeneous ozonation is between first and zero order with respect to both ozone and oxalic acid while at higher ozone gas concentrations, the kinetics was found to be first and zero order with respect to oxalic acid and ozone, respectively. This kinetics is supported through an Eley-Rideal mechanism that involves a surface reaction between non-adsorbed ozone and adsorbed oxalic acid. Apparent activation energies of the homogeneous and heterogeneous catalytic ozonations were found to be 18.2 and 13.6 kcal mol(-1), respectively.

Adsorption↗
PubMed1991

Effect of magnesium on calcium oxalate urolithiasis.

Previous studies have shown that hypomagnesuria induced by magnesium deficient diet causes calcium oxalate crystal deposition in renal tubules of hyperoxaluric rats and administration of magnesium to these rats results in prevention of calcium oxalate crystallization in their kidneys. Based on these studies magnesium was claimed to be beneficial for calcium oxalate stone patients. However, hypomagnesuria is not a common phenomenon. To better understand the role of magnesium as an inhibitor of calcium oxalate crystallization in urine, we studied the effect of magnesium on calcium oxalate urolithiasis in rats on a regular diet and a hyperoxaluric protocol. Excess magnesium was administered to male rats on regular diet and a lithogenic protocol. Magnesium administration to hyperoxaluric rats did not result in significant changes in urinary excretion of calcium or oxalate or in calcium oxalate relative supersaturation. Urinary excretion of citrate was also not significantly altered. Some animals from both groups, those on magnesium therapy and those not on magnesium therapy had crystals deposited in their renal tubules. We conclude that excess magnesium has no significant effect on calcium oxalate urolithiasis in normomagnesuric conditions.

Animals↗
PubMed1982

Clinical manifestations of calcium oxalate monohydrate and dihydrate urolithiasis.

We studied retrospectively 155 patients with calcium oxalate urolithiasis. The patients were divided into 3 groups: 1) those with calcium oxalate monohydrate, 2) those with calcium oxalate dihydrate and 3) those with mixed calcium oxalate monohydrate and dihydrate. Various differences were noted between patients with calcium oxalate monohydrate and those with calcium oxalate dihydrate, with respect to stone characteristics, spontaneous passage of stones, stone recurrence and multiple occurrence. Most important, we noted that patients with calcium oxalate dihydrate had more stone recurrences than patients with calcium oxalate monohydrate.

Adult↗
PubMed1979

Renal failure owing to oxalate nephrosis after jejunoileal bypass.

Oxalate nephrosis resulted in progressive renal failure in 4 patients after jejunoileal bypass for morbid obesity. In general, increased levels of oxalates in the blood and urine of such patients result from enhanced absorption of exogenous oxalates. Urinary calculous formation is determined further by concomitant deficiency of inhibitor substances, whereas oxalate nephrosis probably occurs as a result of oxalate deposition in renal interstitium via the blood stream. Clinical manifestations of oxalate nephrosis include pain, infection, hematuria and renal failure. Routine postoperative renal function studies and early renal biopsy in suspicious cases are urged to establish early diagnosis. Continued deterioration of renal function, despite therapy with oxalate restruction and oxalate binding agents, indicates a reversal of the bypass to preserve unaffected renal substance.

Adult↗
PubMed1999

Oxalic acid production and aluminum tolerance in Pseudomonas fluorescens.

13C NMR studies on intact cells from Al-stressed Pseudomonas fluorescens incubated with citric acid or Al-citrate yielded peaks at 158 and 166 ppm that were attributable to free and complexed oxalic acid, respectively. The presence of oxalic acid was further confirmed with the aid of oxalate oxidase. These peaks were not discernable in experiments performed with cells taken from control cultures. Enzymatic analyses of cell fractions showed the highest production of oxalic acid in the inner membrane fraction of Al-stressed cells incubated with glyoxylate. There was an eight-fold increase in the synthesis of oxalic acid in the inner membrane fraction from the Al-stressed cells compared to the control cells. Although oxalic acid production was observed when citrate, Al-citrate and isocitrate were utilized as substrates, the inner membrane fraction did not mediate the formation of oxalic acid from glycine/pyruvate, glycolic acid, oxaloacetate or ascorbate. These data suggest that the increased oxalic acid production in response to Al stress is effected via the oxidation of glyoxylate.

Aluminum↗
PubMed1984

Plasma oxalate concentration in chronic renal disease.

Plasma oxalate was measured with use of the enzyme oxalate oxidase (EC 1.2.3.4; normal values 3.3 +/- 1.5 mumol/L, n = 24) in 50 patients with different degrees of renal failure. The following mean concentrations +/- SD (in mumol/L) were found: for glomerular diseases, 12.7 +/- 7.8 (n = 21); tubular diseases, 20.4 +/- 14.0 (n = 16); chronic renal failure before dialysis, 32.5 +/- 13.5, and after dialysis, 17.8 +/- 3.8 (n = 10); and primary hyperoxalemia, 72.2 +/- 14.5 14.5 (n = 2). The course of plasma oxalate was followed in one of these two patients after renal transplantation and in a patient recovering from acute tubular necrosis. No significant differences were found between patients with glomerular and tubular disorders. Overall, plasma oxalate was correlated with plasma creatinine in patients with glomerular and tubular diseases and dialysis patients (r = .84, P less than .001). Patients with primary hyperoxalemia had values outside the 95% confidence area of the regression line. It is concluded that the values obtained with this method, although probably still tending to overestimate the true oxalate concentration to some extent, provide reliable information about relative differences in plasma oxalate levels. In patients with terminal renal failure, plasma oxalate sometimes rises to levels at which deposition of calcium oxalate in tissues can occur.

Adolescent↗
PubMed2002

Role of Oxalobacter formigenes in calcium oxalate stone disease: a study from North India.

OBJECTIVE: The present study was performed to detect the presence of an oxalate degrading bacteria Oxalobacter formigenes in the GI tract of calcium oxalate stone patients and normal individuals from North India. Furthermore, the possible relationship of this bacterium with number of stone episodes in this part of the world was also studied. The correlation of the presence or absence of O. formigenes with the urinary oxalate levels was evaluated. METHODS: DNA was extracted from the stool samples of 63 calcium oxalate stone formers and 40 normal individuals. Polymerase chain reaction (PCR) was performed using genus specific primers for O. formigenes. The presence of which was confirmed by Southern blotting. Urinary oxalate levels were tested in each patient. RESULTS: As shown by PCR and Southern blotting, O. formigenes was present in 65% of normal individuals and in 30% of calcium oxalate stone formers. In patients with three or greater than three stone episodes colonies were present only in 5.6% of patients. Oxalate excretion was less in patients colonized with O. formigenes as compared to those with no colonization. CONCLUSION: In North Indian population the absence of O. formigenes can lead to a significant increase in the risk of absorptive hyperoxaluria and resultant recurrent calcium oxalate stone episodes.

Adolescent↗
PubMed2003

Bioavailability of soluble oxalate from tea and the effect of consuming milk with the tea.

OBJECTIVES: To measure the availability of oxalate normally extracted when making tea from two commercially available black teas bought from a supermarket in Christchurch, New Zealand in July 2001. DESIGN, SUBJECTS AND INTERVENTION: A randomized double crossover study. Six students and four staff consumed six cups of each brand of tea both with and without added milk over a 24 h period. A total urine collection was taken for the initial 6 h followed by a further 18 h. The oxalate content of the urine voided was measured using an enzyme kit method and the availability of the soluble oxalate consumed was measured for the 6 h and the total 24 h sample. SETTING: University campus. RESULTS: The mean soluble oxalate content of black tea in the two different commercial tea bags was respectively 6.1 and 6.3 mg soluble oxalate/g tea. The mean availability of the oxalate extracted from tea measured over a 6 h period ranged from 1.9 to 4.7% when tea was consumed without milk. The availability of the soluble oxalate from tea ranged from -3.0 to 2.3% for each of the two brands of tea investigated over a 24 h period. CONCLUSION: These studies show that consuming black tea on a daily basis will lead to a moderate intake of soluble oxalate each day, however the consumption of tea with milk on a regular basis will result in the absorption of very little oxalate from tea.

Adult↗
PubMed2006

Clearance and removal of oxalate in children on intensified dialysis for primary hyperoxaluria type 1.

Patients with end-stage renal failure owing to primary hyperoxaluria type 1 (PH1) receive dialysis while waiting for transplantation. So far, dialysis has not been shown to overcome the problem of ongoing oxalate production and deposition at extrarenal sites. We report on six children with PH1 who had to be dialyzed for a median period of 2.5 years while awaiting liver transplantation. Aiming at preventing oxalate tissue accretion, oxalate mass transfer was studied and dialysis intensified accordingly. Mean plasma oxalate concentration was between 51 and 137 micromol/l. In three of the six patients with a urinary output between 630 and 3140 ml, urinary removal of oxalate was between 5.6 and 12.4 mmol/week/1.73 m2. Hemodialysis (HD) in five of the six patients demonstrated a mean oxalate dialysance between 158 and 444 l/week/1.73 m2. Peritoneal dialysis (PD) in two of the six patients showed mean oxalate clearances of 66 and 103 l/week/1.73 m2. One patient received HD and PD. By adding all modes of elimination, a mean total oxalate mass between 10.1 and 24.1 mmol/week/1.73 m2 was removed. Dialysis is still necessary as a temporary therapy for a number of patients with PH1. Dialysis should be instituted pre-emptively and maximally exploited by intensified HD/PD treatment protocols, without, however, cutting back urinary output.

Child↗
PubMed1970

Microbial growth on oxalate by a route not involving glyoxylate carboligase.

1. The metabolism of oxalate by the pink-pigmented organisms, Pseudomonas AM1, Pseudomonas AM2, Protaminobacter ruber and Pseudomonas extorquens has been compared with that of the non-pigmented Pseudomonas oxalaticus. 2. During growth on oxalate, all the organisms contain oxalyl-CoA decarboxylase, formate dehydrogenase and oxalyl-CoA reductase. This is consistent with oxidation of oxalate to carbon dioxide taking place via oxalyl-CoA, formyl-CoA and formate as intermediates, and also reduction of oxalate to glyoxylate taking place via oxalyl-CoA. 3. The pink-pigmented organisms, when grown on oxalate, contain l-serine-glyoxylate aminotransferase and hydroxypyruvate reductase but do not contain glyoxylate carboligase. The converse of this obtains in oxalate-grown Ps. oxalaticus. This indicates that, in contrast with Ps. oxalaticus, synthesis of C(3) compounds from oxalate by the pink-pigmented organisms occurs by a variant of the ;serine pathway' used by Pseudomonas AM1 during growth on C(1) compounds. 4. Evidence in favour of this scheme is provided by the finding that a mutant of Pseudomonas AM1 that lacks hydroxypyruvate reductase is not able to grow on oxalate.

Bacteria↗
PubMed1994

Formation of the L-cysteine-glyoxylate adduct is the mechanism by which L-cysteine decreases oxalate production from glycollate in rat hepatocytes.

Formation of thiazolidine-2,4-dicarboxylic acid, the L-cysteine-glyoxylate adduct, is the putative mechanism by which L-cysteine reduces hepatic oxalate production from glycollate [Bais, Rofe and Conyers (1991) J. Urol. 145, 1302-1305]. This was investigated in isolated rat hepatocytes by the simultaneous measurement of both adduct and oxalate formation. Different diastereoisomeric ratios of cis- and trans-adduct were prepared and characterized to provide both standard material for the enzymic analysis of adduct in hepatocyte supernatants and to investigate the stability and configuration of the adduct under physiological conditions. In the absence of L-cysteine, hepatocytes produced oxalate from 2 mM glycollate at a rate of 822 +/- 42 nmol/30 min per 10(7) cells. The addition of L-cysteine to the incubation medium at 1.0, 2.5 and 5.0 mM lowered oxalate production by 14 +/- 2, 25 +/- 3 (P < 0.05) and 38 +/- 3% (P < 0.01) respectively. These reductions were accompanied by almost stoichiometric increases in the levels of the adduct: 162 +/- 6, 264 +/- 27 and 363 +/- 30 nmol/30 min per 10(7) cells. Adduct formation is therefore confirmed as the primary mechanism by which L-cysteine decreases oxalate production from glycollate. As urinary oxalate excretion is a prime risk factor in the formation of calcium oxalate stones, any reduction in endogenous oxalate production is of clinical significance in the prevention of this formation.

Animals↗