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PubMed1999

Immunochemical detection of oxalate monoalkylamide, an ascorbate-derived Maillard reaction product in the human lens.

Carbohydrates with reactive aldehyde and ketone groups can undergo Maillard reactions with proteins to form advanced glycation end products. Oxalate monoalkylamide was identified as one of the advanced glycation end products formed from the Maillard reaction of ascorbate with proteins. In these experiments, we have analyzed human lens proteins immunochemically for the presence of oxalate monoalkylamide. Oxalate monoalkylamide was absent in most of the very young lenses but was present in old and cataractous lenses. The highest levels were found in senile brunescent lenses. Incubation experiments using bovine lens proteins revealed that oxalate monoalkylamide could form from the ascorbate degradation products, 2,3-diketogulonate and L-threose. These data provide the first evidence for oxalate monoalkylamide in vivo and suggest that ascorbate degradation and its binding to proteins are enhanced during lens aging and cataract formation.

Adolescent↗

PubMed1992

Ascorbic acid overdosing: a risk factor for calcium oxalate nephrolithiasis.

A total of 15 patients with unilateral nephrostomy tubes after extracorporeal shock wave lithotripsy received either 0 (placebo), 100, 500, 1,000 or 2,000 mg. ascorbic acid on days 2 and 3 postoperatively. Before and after administration, successive 6-hour urine specimens were collected from the nephrostomy tube and from the contralateral kidney directly into a preservative to stabilize ascorbic acid and oxalate. In 1 patient in each group preservative was omitted from the collection pouch. Urinary oxalate was then measured enzymatically after removal of ascorbic acid with sodium nitrite. Preservatives proved necessary for full recovery of analyte. At doses of 500 mg. or more of ascorbic acid there was a statistically significant increase in urinary oxalate equivalent to 1.2 to 1.8% of the millimoles of ascorbate administered. This represented an increase in urinary oxalate excretion of 6 to 13 mg. per day per 1,000 mg. ascorbic acid supplement. This amount would increase the risk of calcium oxalate urolithiasis.

Adult↗

PubMed1988

A new approach to the study of urinary macromolecules as a participant in calcium oxalate crystallization.

Despite intense investigation, the relationship of urinary proteins to urinary stone matrix formation remains poorly understood. In an attempt to gain more information regarding this interaction, the binding of urinary proteins to calcium oxalate crystals formed in urine in vitro was studied. 0.1 M calcium chloride and 0.1 M sodium oxalate were added to an aliquot of urine collected from five non-infected, non-stone forming males. The resulting calcium oxalate crystals were centrifuged and the pellet demineralized with 5% EDTA. Gel filtration chromatography was used to isolate the protein fraction from the urine samples before and after crystallization of calcium oxalate. The proteins recovered from the crystals and urine were separated by two-dimensional polyacrylamide gel electrophoresis. Many, but not all of the urinary proteins were bound by the crystals. Albumin, seen to the most abundant urinary protein, was absent or markedly diminished in all instances, and the second most abundant urinary protein, PC-30, became the predominant protein component of the crystals. An unidentified protein with approximate molecular weight of 22,000 daltons and isoelectric point of 6.4 was highly concentrated by the crystals even when undetected in the urine. The study suggests that the binding of urinary proteins to calcium oxalate crystals formed in urine in vitro is not a random event but rather a selective phenomenon.

Adult↗

PubMed1987

Piridoxilate-induced calcium oxalate calculi: a new drug-induced metabolic nephrolithiasis.

During the last 4 years we collected 27 specimens of calcium oxalate nephrolithiasis in patients receiving long-term treatment with piridoxilate, a drug composed of an equimolar combination of glyoxylate and pyridoxine. The mean duration of treatment was 3.6 years (range 4 months to 10 years) and the mean daily dose was 580 mg. piridoxilate, which contained 160 mg. glyoxylate. Calculi often recurred, with an average number of 9.9 per patient, and an open operation, shock wave lithotripsy or percutaneous nephrolithotomy was required in 22 patients (81 per cent). Oxalate excretion was 727 +/- 246 mumol. per day while on the drug and 382 +/- 201 mumol. per day after the drug was withdrawn. Whewellite was the major component of calculi in all cases but the stones exhibited a peculiar morphological arrangement, with multiple small indentations and a fine mamillary structure. Freshly voided urine specimens contained unusual crystals, which on infrared spectroscopy were composed of calcium oxalate trihydrate, a variety of crystal never observed previously in human urine. Piridoxilate-induced calcium oxalate nephrolithiasis is a new variety of metabolic drug-induced nephrolithiasis. Our observations suggest that even large doses of pyridoxine may be unable to prevent the excessive production of oxalate from glyoxylate.

Adult↗

PubMed1984

Pentosan polysulfate as an inhibitor of calcium oxalate crystal growth.

Pentosan polysulfate was studied as a calcium oxalate crystal growth inhibitor. The inhibition from pentosan polysulfate at concentrations ranging from 3.5 to 110 mg./l. was measured in simple inorganic calcium oxalate solutions at pH 5, 6 and 7. Pentosan polysulfate also was mixed with urine at concentrations from 10 to 350 mg./l. and inhibition determined. Measurement of calcium oxalate crystal growth inhibition was performed in a seeded crystal growth system. One inhibitory unit (concentration of pentosan polysulfate necessary to give a 50 per cent reduction in the rate of crystal growth) was 5.7 +/- 2 mg./l. at pH 5, 7.2 +/- 1.1 mg./l. at pH 6 and 6.0 +/- 2.1 mg./l. at pH 7. Urine-pentosan polysulfate mixtures showed more inhibitory activity than the predicted inhibition present. Addition of pentosan polysulfate to urine at a concentration of 10 mg./l. increased the inhibitory activity from 45 +/- 3 to 59 +/- 3 IU/l. Pentosan polysulfate is a potent calcium oxalate crystal growth inhibitor in urine at physiologic pH levels. If the urinary concentration of pentosan polysulfate after oral administration reaches 10 mg./l., the increase in inhibitory activity in urine that may occur might be important in the treatment of patients who form calcium oxalate calculi within the urinary tract.

Calcium Oxalate↗

PubMed1984

Variations in urine composition during the day in patients with calcium oxalate stone disease.

The diurnal variations of urine composition with respect to calcium, magnesium, oxalate, citrate and inhibition of calcium oxalate crystal growth were studied in patients with recurrent calcium oxalate stone disease. There was considerable variation in the excretion of the different urine constituents with meal-related peaks, which was most pronounced for calcium. The highest concentration of calcium was observed before noon, and between 7 and 11 p.m. Oxalate concentration was highest between 6 and 10 a.m. Consequently, the highest levels of supersaturation were recorded between 6 and 10 a.m., and 6 and 10 p.m. The inhibition index was at the highest level during the first morning hours and could be important in counteracting crystal growth at that time. The risk of exceeding a theoretical formation product of calcium oxalate appeared to be low, with a 24-hour urine volume more than 2,000 ml.

Adult↗

PubMed1977

Oxalate stone disease after intestinal resection.

There have been 543 jejuno-ileal bypass patients screened for the presence of urinary calculi 1 to 6 years postoperatively. Of these patients 9 per cent have had 1 to 2 calculi during the followup and 3 per cent have had multiple calculi. Ninety-four per cent of the recovered calculi consisted entirely of calcium oxalate. Seven patients had a history of stones before the bypass, 6 of whom have had additional stones postoperatively. To define the conditions associated with stone formation in these patients measurements of serum and urinary oxalate concentration, urinary calcium oxalate saturation, urinary crystal size distribution, and the rates of intestinal oxalate absorption and urinary crystallization have been performed on patients who did and did not have stones postoperatively. On the basis of these studies it appears that the patients in whom stones formed differ from those in whom they did not form only in the rate of urinary crystallization and in the number of large crystal particles present in the urine. Evaluation of current therapeutic modalities in terms of the capability to correct these stone-forming characteristics and to reduce actual calculus formation reveals that the only successful regimen is that which includes an extreme reduction of oxalate ingestion.

Follow-Up Studies↗

PubMed1976

Urinary supersaturation with calcium oxalate before and during orthophosphate therapy.

The concentrations of sodium, potassium, calcium, magnesium, phosphorus, sulfate, citrate and oxalate in the urine of normal subjects were compared to the concentrations in urine of calcium oxalate stone-forming patients. Because of the large volume excreted by stone-forming patients the urine contained less concentrations of sodium, potassium, magnesium, phosphorus, sulfate and citrate than did the urine from normal subjects. The urinary concentrations of calcium and oxalate were similar in the 2 groups and, thus, the calculated supersaturation of calcium oxalate was greater in the urine of stone-forming patients than in the urine of normal subjects. Orthophosphate therapy increased the urinary concentration of alkali ions and phosphate but reduced urinary calcium concentration, thereby causing a reduction in urine supersaturation with calcium oxalate. There was no discernible correlation between the phosphate-induced changes in urine supersaturation and the presence or absence of continued calculus formation.

Calcium↗

PubMed1993

Physicochemical considerations in the development and prevention of calcium oxalate urolithiasis.

Calcium oxalate urolithiasis is very common in western societies. In recent years significant progress has been made in identifying and quantitating physico-chemical processes involved in calcium oxalate urinary stone formation. The ability of urine to inhibit the agglomeration of calcium oxalate crystals is an important protective mechanism against stone formation. The process of crystal agglomeration is modulated to a large extent by citrate and it is disturbed in patients with hypocitraturia. Dietary factors, in particular high animal protein intake appear to affect adversely the ability of urine to inhibit calcium oxalate crystal agglomeration. Effective prevention of calcium oxalate urolithiasis should aim at restoring the urine's ability to inhibit the agglomeration of crystals and more emphasis should be given to dietary measures.

Calcium Oxalate↗

PubMed1999

Epidemiology of canine calcium oxalate uroliths. Identifying risk factors.

Calcium oxalate uroliths are most commonly encountered in Miniature Schnauzers, Lhaso Apsos, Yorkshire Terriers, Bichons Frises, Shih Tzus, and Miniature Poodles. They are more common in males than females, and more common in older than young dogs. Dogs that form abnormal nephrocalcin are also predisposed to calcium oxalate uroliths. Dietary risk factors for calcium oxalate uroliths include excessive calcium supplementation or excessive calcium restriction, excessive oxalic acid, high protein, high sodium, restricted phosphorus, restricted potassium, and restricted moisture (dry formulations). Dogs with hyperadrenocorticism or hypercalcemia are predisposed to calcium oxalate urolith formation.

Animals↗

PubMed2003

Heavy atom isotope effects on the reaction catalyzed by the oxalate decarboxylase from Bacillus subtilis.

Oxalate decarboxylase (OxDC) catalyzes a remarkable transformation in which the C-C bond in oxalate is cleaved to give carbon dioxide and formate. Like the native OxDC isolated from Aspergillus niger, the recombinant, bacterial OxDC from Bacillus subtilis contains Mn(II) in its resting state and requires catalytic dioxygen for activity. The most likely mechanism for OxDC-catalyzed C-C bond cleavage involves the participation of free radical intermediates, although this hypothesis remains to be unequivocally demonstrated. Efforts to delineate the catalytic mechanism have been placed on a firm foundation by the high-resolution crystal structure of recombinant, wild type B. subtilis OxDC (Anand et al., Biochemistry 2002, 41, 7659-7669). We now report the results of heavy-atom kinetic isotope effect measurements for the OxDC-catalyzed decarboxylation of oxalate, in what appear to be the first detailed studies of the mechanism employed by OxDC. At pH 4.2, the OxDC-catalyzed formation of formate and CO(2) have normal (13)C isotope effects of 1.5% +/- 0.1% and 0.5% +/- 0.1%, respectively, while the (18)O isotope effect on the formation of formate is 1.1% +/- 0.2% normal. Similarly at pH 5.7, the production of formate and CO(2) exhibits normal (13)C isotope effects of 1.9% +/- 0.1% and 0.8% +/- 0.1%, respectively, and the (18)O isotope effect on the formation of formate is 1.0% +/- 0.2% normal. The (18)O isotope effect on the formation of CO(2), however, 0.7% +/- 0.2%, is inverse at pH 5.7. These results are consistent with a multistep model in which a reversible, proton-coupled, electron transfer from bound oxalate to the Mn-enzyme gives an oxalate radical, which decarboxylates to yield a formate radical anion. Subsequent reduction and protonation of this intermediate then gives formate.

Bacillus subtilis↗

PubMed1979

Experimental oxalate urolith formation in rats.

Urinary calculi composed of calcium oxalate were produced in male hooded Wistar rats fed a vitamin B6 deficient diet over 16 weeks. This basic diet was modified by doubling the phosphate content or loading with vitamin C or D3 in three treatment groups. The number of rats developing oxalate stones was not altered by the addition of vitamin D3 or phosphate, but there was a significant increase in total weight of stone formed and histological evidence of extensive renal damage in rats on the high vitamin D3 diet. The addition of vitamin C to the vitamin B6 deficient rats resulted in a reduction in the number of rats with uroliths and a fall in urinary oxalate excretion, while similarly loaded vitamin B6 supplemented controls were free of oxalate calculi. It is concluded that the oxalate urolithiasis induced by vitamin B6 deficiency was exacerbated by added vitamin D3 and reduced by vitamin C.

Animals↗

PubMed1975

Effect of diphosphonate on crystallization of calcium oxalate in vitro.

Reliable techniques for the calculation of activity product (state of saturation), formation product (limit of metastability) and crystal growth of calcium oxalate were devised. The activity product at saturation was 2.53 times 10 minus 9 M2, and was independent of duration of incubation, solid-to-solution ratio, pH, calcium concentration or ionic strength. These tehcniques were utilized to assess the effect of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP) on crystallization of calcium oxalate in an aqueous salt solution in vitro. EHDP increased the formation product of calcium oxalate, indicating an inhibition of nucleation of calcium oxalate. Further, it inhibited the crystal growth of calcium oxalate.

Calcium↗

PubMed1982

Pathogenesis and clinical course of mixed calcium oxalate and uric acid nephrolithiasis.

By direct measurement, urine from patients who form calcium oxalate stones was supersaturated abnormally with respect to calcium oxalate monohydrate but not supersaturated with respect to undissociated uric acid. Urine from patients who form uric acid stones was supersaturated excessively with undissociated uric acid but not calcium oxalate. Patients who form both calcium oxalate and uric acid stones, however, produce urine that is supersaturated with respect to both solid phases. Low urine pH was the primary factor that increased supersaturation with respect to undissociated uric acid. The formation of both calcium oxalate and uric acid stones appears to be explained by a dual abnormality of urine supersaturation.

Calcium Oxalate↗

PubMed1984

Calcium oxalate dihydrate formation in urine.

Factors that promote the formation of calcium oxalate dihydrate (COD) in urine were investigated. Crystals resulting from the incubation of 25-ml aliquots of the solution to be tested and 1 ml of 0.05 M ammonium oxalate were examined by infrared spectrophotometry. With reference spectra of known mixtures, the fractional content of COD could be estimated. At pH 6.5, only COD formed in human urine. In a supersaturated inorganic solution of calcium oxalate, the percentage of COD was 7.5 +/- 1.4. Pyrophosphate (1 to 8 X 10(-5) M), citrate (10(-4) to 2 X 10(-3) M), RNA from yeast (5 X 10(-9) to 0.5 X 10(-7) M), or heparin (2 X 10(-9) to 2 X 10(-7) M) added to a supersaturated solution of calcium oxalate increased the percentage of COD proportional to the concentration of the additives. Chondroitin sulfate and magnesium had no effect. An increase in pH increased the formation of COD in inorganic solutions containing citrate, pyrophosphate, and heparin and in undiluted urine. RNA-citrates and citrate-pyrophosphate mixtures showed additivity. Urine showed an effect that was inversely proportional to its dilution. Substances that promote COD formation in this system had their phase-stabilizing effects at concentrations normally found in urine. Further, these same substances are known inhibitors of calcium oxalate crystal formation. With both inhibition and phase stabilization, there is additivity of effects, and changes in pH alter the response.

Adult↗

PubMed2005

Manganese(II) chemistry of a new N3O-donor chelate ligand: synthesis, X-ray structures, and magnetic properties of solvent- and oxalate-bound complexes.

The synthesis and characterization of a new N3O donor ligand N-benzyl-N-((6-pivaloylamido-2-pyridyl)methyl)-N-(2-pyridylmethyl)amine (bpppa) is reported. Treatment of bpppa with Mn(II)(ClO4)2.6H2O in acetonitrile solution yielded the mononuclear [(bpppa)Mn(CH3CN)(H2O)](ClO4)2 (1) which was characterized by X-ray crystallography, elemental analysis, IR spectroscopy, mass spectrometry, and a solution magnetic moment measurement. Admixture of equimolar equivalents of bpppa and Mn(II)(ClO4)2.6H2O in methanol solution, followed by addition of 0.5 or 1 equivalents of sodium oxalate, yielded the binuclear complex [{(bpppa)Mn}2([mu]-C2O4)](ClO4)2 (2), which was characterized by X-ray crystallography, elemental analysis, IR spectroscopy, mass spectrometry, and solid-state magnetic measurements. While 1 is mononuclear, the formation of the binuclear oxalate derivative indicates that use of the bpppa ligand does not enable isolation of a complex that is structurally relevant to a proposed 1:1 Mn(II)-oxalate adduct in the catalytic cycle of the oxalate degrading enzyme oxalate decarboxylase.

Benzyl Compounds↗

PubMed1965

The fluorimetric determination of oxalic acid in blood and other biological materials.

1. Oxalic acid is separated from interfering substances by extraction with tri-n-butyl phosphate followed by co-precipitation with calcium sulphate. The precipitated oxalic acid is then reduced to glyoxylic acid, which is coupled with resorcinol to form a coloured fluorescent complex. 2. The spectrofluorometric method described is sensitive and highly specific, the minimum detectable amount of oxalic acid being 0.9mumole under the recommended conditions. 3. The concentration of oxalic acid in blood from 15 normal adults was 200-320mug./100ml. For serum the range was 135-280mug./100ml. The urinary excretion of oxalic acid by 60 normal adults on a normal diet was 9.0-28.5mg./24hr.

Blood Chemical Analysis↗

PubMed2002

Cloning and characterization of the 5'-flanking region of the oxalate decarboxylase gene from Flammulina velutipes.

The oxalate-degrading enzyme, oxalate decarboxylase (OXDC), was purified and characterized from Flammulina velutipes, a basidiomycetous fungus [Mehta and Datta (1991) J. Biol. Chem. 266, 23548-23553]. The cDNA cloning and analyses revealed that OXDC transcription was induced by oxalic acid. However, in this report, we show that OXDC transcription is induced by low pH, not by oxalate. To understand the regulatory mechanism of OXDC expression, we have cloned and analysed a 580-bp genomic fragment from the 5'-flanking region of the OXDC gene. Sequence analysis showed the presence of several eukaryotic transcription factor binding motifs within the -580 bp of the upstream region. Electrophoretic-mobility-shift assays with partially purified cell extracts revealed specific binding of a factor in acid-induced, but not in uninduced, extracts. Furthermore, DNase I protection assays using the partially purified fraction from oxalic acid-induced extract revealed a footprint of a 13-bp sequence 5'GCGGGGTCGCCGA3', termed low pH responsive element (LPRE), corresponding to the -287 to -275 bp region of the OXDC promoter. Our results suggest that in F. velutipes cells, activation of OXDC transcription in response to low pH is mediated by the binding of a novel transcription factor through the LPRE site in the OXDC promoter.

Agaricales↗