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PubMed2002

Effect of cyclosporin A treatment on renal calcium oxalate binding in experimental hyperoxaluria.

This study was aimed to investigate the effect ofCyclosporin A administration on renal calcium oxalate binding under hyperoxaluric condition. Cyclosporin A administration or ammonium oxalate treatment increased calcium oxalate binding, which was further increased in kidney treated with cyclosporin A and ammonium oxalate together. The increase of calcium oxalate binding was associated with lipid peroxidation as well as with a concomitant decrease in total thiol in both rat and human kdiney homogenate. Cyclosporin A administration to hyperoxaluric rats resulted with increased calcium oxalate binding protein. However there was no change with specific activity of the protein. In conclusion, Cyclosporin A administration either to normal or hyperoxaluric rats is resulted with increased concentration of calcium oxalate binding protein as well as enhanced activity due to membrane lipid peroxidation.

Animals↗
PubMed2001

A physiological role for oxalic acid biosynthesis in the wood-rotting basidiomycete Fomitopsis palustris.

A metabolic mechanism for oxalic acid biosynthesis in the wood-rotting basidiomycete Fomitopsis palustris has been proposed on the basis of biochemical analyses of glucose metabolism. There was a strong correlation between glucose consumption and oxalate production. Oxalic acid was found to accumulate in the culture fluid in about 80% of the theoretical yield or about 5-fold, on the basis of the fungal biomass harvested. The results clearly indicate that glucose was not completely oxidized to CO(2) by the tricarboxylic acid (TCA) cycle but converted mainly to oxalate. The determination of the 12 enzymes concerned has revealed the occurrence of the unprecedented metabolic coupling of the TCA and glyoxylate cycles that support oxalate biosynthesis. In this metabolic system, isocitrate lyase (EC ), together with oxaloacetase (EC ), was found to play a pivotal role in yielding oxalate from oxaloacetate via the acetate-recycling routes. Moreover, malate dehydrogenase (EC ), with an extraordinarily high activity among the enzymes tested, was shown to play an important role in generating NADH by oxidation of malate to oxaloacetate. Thus, it is proposed that the wood-rotting basidiomycete acquires biochemical energy by oxidizing glucose to oxalate.

Basidiomycota↗
PubMed1988

Plasma oxalate concentration and secondary oxalosis in patients with chronic renal failure.

To examine the association between hyperoxalaemia and secondary oxalosis, measurement of plasma oxalate concentration was combined with a search for tissue deposition of calcium oxalate crystals in patients with chronic renal disease. Two groups of patients were studied. In the first, samples of the inferior epigastric artery were taken from 35 patients at the time of renal transplantation. In the second, sections taken at necropsy from 23 patients with chronic renal failure in whom plasma oxalate had been measured before death were examined. Though plasma oxalate concentrations ranged between 6 and 116 mumol/l (four to 78 times greater than the upper limit of the reference range), no extrarenal deposits of oxalate were found in either study. Renal deposition of oxalate was associated with a plasma oxalate concentration of greater than 20 mumol/l. This study gives no support to the suggestion that hyperoxalaemia of the degree seen in patients with the type of chronic renal failure that is not due to primary hyperoxaluria confers an appreciable risk of extrarenal oxalosis.

Adolescent↗
PubMed2005

Effect of hyperprotidic diet associated or not with hypercalcic diet on calcium oxalate stone formation in rat.

The aim of this study was to determine whether protein, administered alone or simultaneously with a hypercalcic diet, was able to aggravate calcium oxalate stone formation in rats. Thirty-two male Wistar rats were randomly divided into four groups of 8 rats each and assigned a calcium oxalate lithogenic diet added to their drinking water for 3 weeks. One group, used as reference, received a standard diet prepared in our laboratory. The second was assigned the same diet but supplemented with 7.5 g animal proteins/100 g diet. The third received a diet containing 500 mg calcium more than the standard group. The diet given to the last group was supplemented with calcium and protein at the same doses indicated previously. One day before the end of treatment, each animal was placed in a metabolic cage to collect 24-hour urine samples and determine urinary creatinine, urea, calcium, magnesium, phosphate, uric acid, citric acid and oxalate levels. Immediately thereafter, aortic blood was collected to determine the same parameters as in urine. The kidneys were also removed to determine calcium oxalate deposits. Our results showed an increased 24-hour urinary excretion of calcium, oxalate and uric acid and decreased urinary citric acid excretion only in groups that received protein supplementation. At the same time, calcium oxalate deposits were found significantly higher in hyperprotidic diets than reference or calcium-supplemented groups. According to these findings, glomerular filtration, fractional excretion of urea and reabsorption of water, calcium and magnesium were found significantly lower in hyperprotidic diets compared to other groups. These results demonstrate that proteins could seriously aggravate calcium oxalate stones and cause renal disturbances.

Animals↗
PubMed1985

Critical role of oxalate restriction in association with calcium restriction to decrease the probability of being a stone former: insufficient effect in idiopathic hypercalciuria.

The probability of being a stone former (PSF) was calculated in 3 groups of idiopathic calcium stone formers [with normocalciuria (NC), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH)] in 4 conditions: while on a free diet; on a calcium- and oxalate-restricted diet during 4 days; after an oxalate load, while on a 1.5-gram calcium diet, and after an oxalate load while on a calcium-restricted diet. Combined calcium and oxalate restriction significantly decreased PSF only in NC and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater during a calcium-restricted diet than during the 1.5-gram calcium diet in all groups of patients (4, 6 and 12 times greater in NC, DH and IH, respectively). These data show the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. This combined restriction is however not sufficient in idiopathic hypercalciuric patients to decrease their PSF.

Calcium↗
PubMed2003

Mechanisms mediating oxalate-induced alterations in renal cell functions.

Oxalate is a major component of the most common form of kidney stones--calcium oxalate stones. High concentrations of oxalate promote stone formation in two ways: (1) by providing urinary conditions favorable to the formation of calcium oxalate crystals, and (2) by inducing renal injury that generates cellular debris and promotes crystal nucleation and attachment. Oxalate toxicity is mediated in part by activation of lipid signaling pathways that produce arachidonic acid, lysophospholipids, and ceramide. These lipids disrupt mitochondrial function by increasing reactive oxygen species (ROS), decreasing mitochondrial membrane potential, and increasing mitochondrial permeability. The net response is cytochrome C release, activation of caspases, and apoptosis or necrosis. Not all cells succumb to oxalate toxicity, however, in those cells that don't, ROS and lipid-signaling molecules induce changes in gene expression that allow them to survive and adapt to the toxic insult. The increased expression of immediate early genes (IEGs), osteopontin, extracellular matrix (ECM) proteins, crystallization inhibitors, and chemokines orchestrates a group of cellular responses--including cell proliferation, secretion of kidney stone inhibitory proteins, recruitment of immune cells, and tissue remodeling--that limit accumulation of cell debris or increase the production of inhibitors of calcium oxalate crystallization, thereby limiting stone formation.

Adaptation, Physiological↗
PubMed1981

The fate of oxalic acid in the Wistar rat.

1. An established procedure for determining oxalate in human urine has been modified for rat urine. The daily excretion of oxalate by the male Wistar rat is 570-650 microgram. 2. Oxalate excretion in rat urine following i.p. administration of [14C]oxalic acid (1-70 mg/kg) has been studied. The rate and degree of excretion are dose-dependent. 3. The excretion of urinary oxalate by the rat has been quantified after administration of two oxalate-producing xenobiotics, alpha-chlorohydrin and 1,2-dibromo-3-chloropropane. 4. Oxalate inhibits the metabolism of glucose and lactate by isolated rat kidney tubules in vitro.

Animals↗
PubMed1991

A simple method for quantitating the propensity for calcium oxalate crystallization in urine.

To assess the propensity for spontaneous crystallization of calcium oxalate in urine, the permissible increment in oxalate is calculated. The previous method required visual observation of crystallization with the addition of oxalate, this warranted the need for a large volume of urine and a sacrifice in accuracy in defining differences between small incremental changes of added oxalate. Therefore, this method has been miniaturized and spontaneous crystallization is detected from the depletion of radioactive oxalate. The new "micro" method demonstrated a marked decrease (p < 0.001) in the permissible increment in oxalate in urine of stone formers versus normal subjects. Moreover, crystallization inhibitors added to urine, in vitro (heparin or diphosphonate) or in vivo (potassium citrate administration), substantially increased the permissible increment in oxalate. Thus, the "micro" method has proven reliable and accurate in discriminating stone forming from control urine and in distinguishing changes of inhibitory activity.

Adult↗
PubMed1990

Oxalate molecule as the trap for gamma-irradiation energy in the amorphous aluminosilicate Al2(OH)6H4SiO4.

Paramagnetic species which were the products of gamma irradiation at 77 K and at room temperature were studied by ESR spectroscopy in the amorphous aluminosilicate, Al2(OH)6H4SiO4, prepared in the presence and in the absence of oxalate ion. The aluminosilicate precipitated from the solution containing the oxalate ion in 10(-4) mol dm-3 concentration contained the oxalate only in trace amounts. When gamma-irradiated at 77 K and at room temperature, this compound gave the stable paramagnetic species represented by the single ESR line centered at g = 2.000. We ascribe this spectrum to the CO2- radical formed from the oxalate ion. The same aluminosilicate prepared in the absence of the oxalate either produced no stable paramagnetic product after gamma irradiation at room temperature or resulted in composite ESR spectra, indicating the presence of several paramagnetic species if irradiated at 77 K. Complex ESR spectra were transformed by heating to the stable paramagnetic centers which differed from the one obtained from oxalate ion. We conclude that in Al2(OH)6H4SiO4 oxalate acts as a trap for the gamma-radiation energy.

Aluminum Silicates↗
PubMed1988

Intestinal absorption of oxalic acid in ileostomized patients.

The diagnostic usefulness of an intestinal oxalic acid absorption test was evaluated in nine patients with ileostomy. They received an oral overload of 250 mg sodium oxalate and 4 Ci oxalic acid-C14 and a controlled diet. The urinary levels of cold and radioactive oxalic acid were measured 24 and 48 hours after the overload. Intestinal oxalic acid absorption in the ileostomized patients was found to be normal, with 16.13 +/- 5.1% of the administered dose being eliminated/recovered in the urine 48 hours after the overload (control value = 14.5 +/- 2.8%). The dose of radioactivity excreted on the second day after the overload was smaller in the ileostomy group than in the control group, possibly connected with the absence of colon. The results suggest that in ileostomized patients whose colon has been removed, oxalic acid absorption is normal. Hence there appears to be no risk of oxalic lithiasis in this group.

Adult↗
PubMedDate not supplied

Gas chromatographic determination of oxalic acid in foods.

A new quantitative gas chromatographic (GC) method has been developed for the determination of oxalic acid in foods. Solid sample is extracted with water (soluble oxalic acid) or 2N hydrochloric acid (total oxalic acid) at room temperature. An aliquot of sample extract is evaporated to dryness, and the oxalic acid in the residue is methylated with 7% hydrochloric acid-methanol. The reaction mixture is extracted with chloroform, and dimethyl oxalate is quantitated by GC. Recovery of oxalic acid added to liquid samples averaged 100.6%; recoveries from extracts of solid samples were 96.2-99.5 and 97.2-100.1% for water and hydrochloric acid extractions, respectively. Results are shown for determination of oxalic acid in spinach and beverages. The technique is simple, rapid, and accurate, and small samples may be used. The limit of determination is 20 micrograms.

Beverages↗
PubMed1984

Determination of urinary oxalate by ion chromatography: some modifications.

Ion chromatography was used to determine urinary oxalate concentration. The minimal detectable limit in a standard solution was 0.02 microgram/ml, and the regression line for the standard curve from 0.5 to 10 micrograms/ml had a significant correlation coefficient (p less than 0.01), but it was difficult to obtain reproducible results with ion chromatography. There were two obstacles: Urine was always oversaturated with calcium oxalate, and the presence of sulfate, the peak of which is next to the oxalate peak on the chromatogram of urine, seemed to interfere with oxalate conductivity. Comparison of 4 different dilutions of urine showed that the oxalate conductivity was highest in the 100-fold dilution and decreased gradually with increasing concentration. The conductivity of the oxalate standard (1 microgram/ml) also decreased as the concentration of sulfate increased. Therefore, it was concluded that to obtain reproducible results urine should be diluted 100-fold and that a recovery test by adding 0.25 microgram/ml oxalic acid should be performed on all urine samples.

Calcium Oxalate↗
PubMed1984

Effect of large intake of ascorbic acid on urinary and plasma oxalic acid levels.

Blood samples form ten healthy subjects, who had been ingesting 3-10 g of ascorbic acid for at least two years, were collected. The ascorbic acid and oxalic acid levels in the plasma of these subjects were measured. The concentrations of oxalic acid in these plasma samples are within the range of plasma oxalate levels of human subjects who were not ingesting ascorbic acid supplements. Large quantities of ascorbic acid (10 g/day) were administered to healthy human subjects. Daily urinary samples of these subjects were collected before and during treatment. Urinary ascorbic acid and oxalic acid levels of these samples were measured. Among the six subjects tested, five experienced no significant change on urinary oxalate excretion. Urinary oxalate level of one subject was significantly elevated upon the large intake of ascorbic acid. But the increased daily excretion of oxylate in this subject is within the changes in urinary oxalate content from consuming normal diets.

Adult↗
PubMed1984

[Monohydrate and dihydrate oxalic lithiasis. Calculi, their macroscopic structure (radiographic and therapeutic impact). Calciuria and oxaluria].

Calculi of pure calcium oxalate monohydroxide are hard, polish, dark brown stones, of a very tenuous crystalline structure. On the contrary, calculi of pure bihydroxide oxalate are clear irregular stones with a spiky surface. They are more friable and less hard than monohydroxide oxalate stones. Monohydroxide oxalate stones radiologically are regular and homogeneous, whereas bihydroxide oxalate stones have an irregular aspect. Monohydroxide oxalic lithiasis is less frequent than bihydroxide oxalic lithiasis. The proportion of monohydroxide lithiasis is the same in men and women whereas bihydroxide lithiasis is more frequent in men. Of a biologic point of view, in monohydroxide lithiasis, calciuria and oxaluria are often normal while proportion of hypercalciuria and hyperoxaluria is more important in bihydroxide lithiasis. Evolutivity is clearly inferior in monohydroxide lithiasis than in bihydroxide lithiasis.

Adult↗
PubMed1983

On the oxalate stimulation of ATP-dependent calcium accumulation by smooth muscle subcellular membranes.

Subcellular distribution of azide-insensitive, ATP-dependent Ca -accumulation in the presence and absence of 5 mM oxalate by fractions isolated from several different types of smooth muscle were studied. Although oxalate stimulated the Ca -accumulation to various degrees depending upon the source of smooth muscle used, there was no clear association between the stimulatory effect of oxalate and the distribution of any of the enzyme activities used as markers for various membranes. The distribution of ATP-dependent Ca -accumulation in the absence of oxalate, on the other hand, correlates relatively well with that of the plasma membrane marker in spite of reduced total recovery of the Ca -accumulation compared to those of the protein content and membrane markers. However, a greater reduction in the total percent recovery of the ATP-dependent Ca accumulation by fraction from three different types of smooth muscle was consistently observed when carried out in the presence compared to the absence of oxalate. The discrepancy in the total percent recovery of the Ca -accumulation in the presence and absence of oxalate poses a major concern on the uses of oxalate stimulated, ATP-dependent Ca accumulations as a subcellular membrane marker.

Adenosine Triphosphate↗
PubMed1995

Measurement of urinary oxalate and citrate by capillary electrophoresis and indirect ultraviolet absorbance.

We describe a method for measuring urinary oxalate and citrate with capillary electrophoresis (CE) and indirect ultraviolet absorbance detection. Sample preparation is minimal, requiring an acidification, brief centrifugation, and dilution. The method is rapid, with oxalate and citrate having mean migration times of 4.02 and 4.50 min, respectively. The minimal detectable concentration (signal-to-noise ratio of 7) of both oxalate and citrate in urine was 7 mg/L. Total imprecisions (CV) were 1.2-5.6% for three urine samples with oxalate and citrate concentrations of 8-60 mg/L and 80-860 mg/L, respectively. The recovery of added oxalate ranged from 94% to 101%. Results of CE analyses agreed well with enzymatic determinations of oxalate and citrate. Rapid analysis time, accuracy, and reproducibility make this procedure well suited for routine urinary oxalate and citrate determinations.

Capillary Action↗
PubMed1996

Selective inhibition of oxalate-stimulated Ca2+ transport by cyclopiazonic acid and thapsigargin in smooth muscle microsomes.

45Ca2+ uptake and efflux studies were performed on membranes prepared from dog mesenteric artery and rat vas deferens. Oxalate-stimulated, ATP-dependent Ca2+ uptake in microsomal vesicles, a property characteristic of sarcoplasmic reticulum, was completely inhibited in a concentration-dependent manner by cyclopiazonic acid (0.1-30 microM) and thapsigargin (10 nM-10 microM). Using discontinuous sucrose gradient centrifugation, rat vas deferens microsomes were separated into two fractions, one enriched in plasma membrane (F2), the other enriched in sarcoplasmic reticulum (F3). The F3 fraction had a major increase in Ca2+ uptake in the presence of oxalate, which was completely inhibited by either cyclopiazonic acid or thapsigargin. In the F2 fraction Ca2+ uptake in the presence of oxalate was lower than in F3 and was not completely inhibited by thapsigargin and cyclopiazonic acid. Instead, the F2 fraction had a thapsigargin-insensitive and cyclopiazonic acid insensitive, saponin-sensitive component of uptake, which probably represents Ca2+ uptake by plasma membrane. In the absence of oxalate, the inhibition of Ca2+ uptake by saponin and cyclopiazonic acid or thapsigargin was additive in the F2 and F3 fractions, suggesting that cyclopiazonic acid and thapsigargin selectively inhibited sarcoplasmic reticulum derived Ca2+ uptake and did not affect plasma membrane derived Ca2+ uptake. Measurement of the initial rate of Ca2+ uptake in the presence and absence of oxalate by rat vas deferens microsomes demonstrated selective inhibition of oxalate-stimulated Ca2+ uptake by cyclopiazonic acid and thapsigargin. Ca2+ efflux from rat vas deferens microsomes actively loaded with 45Ca2+ either in presence or the absence of oxalate was not increased by cyclopiazonic acid or thapsigargin, showing that the inhibition of Ca2+ accumulation was not due to an increase in Ca2+ efflux. In both rat vas deferens and dog mesenteric artery, the maximal inhibitory effects of cyclopiazonic acid developed rapidly, whereas for maximal inhibition thapsigargin required pretreatment of microsomes prior to measurement of Ca2+ uptake. In rat vas deferens microsomes the inhibitory effects of cyclopiazonic acid could be quickly and completely reversed, whereas the effects of thapsigargin were not easily reversed. Collectively, these results suggest selectivity of cyclopiazonic acid and thapsigargin for the sarcoplasmic reticulum Ca2+ pump. Their selective inhibitory properties and differences in onset and offset of inhibition make cyclopiazonic acid thapsigargin useful pharmacological tools in the study of the physiological and pathophysiological roles of the sarcoplasmic reticulum Ca2+ pump in regulating smooth muscle Ca2+.

Aminoisobutyric Acids↗
PubMed1996

[Urinary oxalic acid excretion in chronic kidney failure and after kidney transplantation].

Urinary oxalic acid excretion was examined in 61 patients with chronic nephropathies and in 21 patients after renal transplantation with a varying mean glomerular filtration. In both groups of patients a correlation was found between the plasma oxalic acid and serum creatinine and by a hyperbolic correlation between plasma oxalic acid and creatinine clearance. Moreover the authors found a direct correlation between oxalic acid and FEoxalic acid and FE(Na)+, FEH20 and FE1-ascorbic acid in both patient groups. Various chronic nephropathies and treatment in both groups did not affect the revealed correlations. In 13 healthy subjects during the period of maximum water diuresis urinary Na+ excretion did not increase but there was a significant increase of the l-ascorbic acid and oxalic acid excretion. In a group of 8 patients in the polyuric stage of chronic renal failure without dialysis treatment under conditions of increased dietary NaCl intake (15 g/24 h) a significant increase of the urinary Na+ excretion was recorded while the l-ascorbic acid and oxalic acid excretion was unaltered. From the assembled values of the examined biochemical indicators ensues that urinary oxalic acid excretion, similarly as ascorbic acid excretion, depended on water excretion.

Adult↗