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PubMed1982

Inhibitory activity of human urine on calcium oxalate crystal growth: effects of sodium urate and uric acid.

1. Freshly voided urine from healthy subjects was pooled and ultrafiltered (10,000 daltons). The ultrafiltrable and the macromolecular portions were preincubated with calcium oxalate, uric acid and sodium urate crystals and the effects on the inhibitory activity of calcium oxalate crystal growth assessed by monitoring the disappearance of [14C]oxalate from the solution. 2. The inhibitory activity of the ultrafiltrate was higher than that of the urinary macromolecular fraction. Both uninhibited and inhibited crystal growth processes followed second-order kinetics. 3. Calcium oxalate crystals adsorbed almost all the urinary macromolecular inhibitors whereas sodium urate or uric acid crystals adsorbed only 10-20%. 4. In the presence of a metastable solution of calcium oxalate, the incubation of the urinary macromolecular fraction with sodium urate crystals caused a pronounced reduction in the inhibitory activity. A similar effect was seen with uric acid crystals, but to a lesser degree. 5. We conclude that the effect of sodium urate or uric acid crystals alone on naturally occurring urinary macromolecular inhibitors of calcium oxalate crystal growth is weak, but that in the presence of metastable calcium oxalate this is greatly enhanced. A substantial adsorption of the inhibitors on to the crystals is suggested, possibly secondary to epitaxial growth of calcium oxalate on the surface of the urate crystals.

Calcium Oxalate↗
PubMed1990

Effect of urate on calcium oxalate crystallization in human urine: evidence for a promotory role of hyperuricosuria in urolithiasis.

1. The effect of hyperuricosuria, simulated by increasing the concentration of dissolved urate, on the crystallization of calcium oxalate in human urine was examined. 2. Twenty urine samples were studied. Ten of these, designated type A, spontaneously precipitated calcium oxalate dihydrate crystals upon the addition of a solution of sodium urate solution which raised the median urate concentration from 3.1 to 7.0 mmol/l. 3. Adding dissolved urate to the remaining type B samples raised the median urate concentration from 2.2 to 6.2 mmol/l, but did not cause the precipitation of calcium oxalate. This was induced in these samples by the addition of a standard load of oxalate above an empirically determined metastable limit. 4. In the type B urine samples, the addition of urate decreased the median metastable limit from 125 to 66 mumol of oxalate, trebled the median volume of crystalline calcium oxalate deposited from 35,000 to 105,000 microns3/microliters and significantly increased the overall size of the particles precipitated. Calcium oxalate monohydrate was exclusively precipitated, and the individual crystals deposited in the presence of urate were markedly smaller, more numerous, and more highly aggregated than those produced in its absence. 5. These results constitute the most convincing evidence yet obtained that hyperuricosuria may be a powerful promoter of calcium oxalate stone formation.

Adult↗
PubMed1991

Serum calcium oxalate saturation in patients on maintenance haemodialysis for primary hyperoxaluria or oxalosis-unrelated renal diseases.

1. The serum oxalate concentration rises in chronic renal failure and it is only partially eliminated by regular dialysis treatment. However, the recent literature is not conclusive on whether progressive oxalate retention and secondary oxalosis should be expected in patients on regular dialysis treatment. 2. To further investigate this, we have estimated the state of saturation with respect to calcium oxalate monohydrate in plasma ultrafiltrates from 28 patients on maintenance haemodialysis and eight healthy control subjects, matched for sex and age. Five patients had type I primary hyperoxaluria and histologically proven oxalosis, whereas 23 had oxalosis-unrelated renal diseases. Dialysis efficiency was quantified as the KdTd/V of urea. Samples were obtained from each patient before, immediately after and 48 h after a dialysis session. Fasting samples were obtained from the control subjects. Oxalate was determined in both plasma ultrafiltrates and the whole dialysate by ion-exchange chromatography, after a non-delayed and [14C]oxalate-recovery-controlled procedure. The state of saturation with calcium oxalate monohydrate was estimated by means of a computer system which solved the interactions among 45 complex species. 3. The fasting plasma oxalate concentration (means +/- SD) in ultrafiltrates from healthy subjects was 3.8 +/- 1.5 (range 1.4-5.8) mumol/l, and the state of saturation with calcium oxalate monohydrate was 0.096 +/- 0.04.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Do thiazides reduce intestinal oxalate absorption?: a study in vitro using rabbit colon.

1. The purpose of the present study was to examine the effects of various diuretics on intestinal oxalate transport. Transmural oxalate fluxes were measured across isolated, short-circuited tissue segments removed from rabbits and placed in Ussing chambers. 2. The net absorptive flux of oxalate across the distal colon was significantly reduced in the presence of trichlormethiazide at 10(-4) mol/l. In contrast, this diuretic had no effect on oxalate transport in the other intestinal segments examined. Several of the thiazide diuretics tested had some inhibitory effect on colonic oxalate absorption, but at higher concentrations of 10(-3) mol/l or 10(-2) mol/l. 3. We conclude that the previously reported hypooxaluric effects of hydrochlorothiazide and chlorthalidone are most likely not the result of an exclusive or primary effect on intestinal oxalate transport. It is suggested that the reduction in colonic oxalate absorption that was observed with the thiazides probably involves the transport system responsible for oxalate efflux across the basolateral membrane of the colonocyte.

Animals↗
PubMed2003

Concentration gradient of oxalate from cortex to papilla in rat kidney.

BACKGROUND: The kidney eliminates the major fraction of plasma oxalate. It is well known that oxalate is freely filtered by glomeruli and secreted by the proximal tubules. However, the renal handling of oxalate in distal nephrons, which is considered as playing an important role in stone formation, remains obscure. METHODS: At 15-180 min after intravenous injection of 14C-oxalate to rats, the intrarenal localization of radioactivity was quantitatively measured by the radioluminographic method using a bioimaging analyzer. Tissue radioactivity was compared with plasma, and urinary radioactivities were measured by a liquid scintillation counter. The control study was conducted with 14C-inulin. RESULTS: The radioactivity of 14C-oxalate in the papilla was 10 times greater than in the cortex and eight times greater than in the medulla 180 min after injection when almost no radioactivity was present in the urine. In contrast, the radioactivity of 14C-inulin was nine times less in the papilla than in the cortex at the same time. CONCLUSION: Oxalate remains in the renal papilla for an extended period. This accumulation of oxalate may be attributed to calcium oxalate crystal fixation along the deep nephron which is considered to be the first step of stone formation.

Animals↗
PubMed2004

The effect of oral administration of calcium and magnesium on intestinal oxalate absorption in humans.

Calcium oxalate (CaOx) urolithiasis is the most common urinary stone disease (70-75 % of all stones consist of CaOx in countries with western diet). Oxalate is the most lithogenic substance in CaOx crystallisation in urine. Oxalate is either synthesized within the body or absorbed from food. As oxalate is not metabolized in the human body, it appears unchanged in urine. Conventional analysis methods cannot distinguish between endogenous and exogenous oxalate. Our [13C2]oxalate absorption test enabled measurement of intestinal oxalate absorption and quantification of the influence of Ca- and Mg-supplementation on it. The effects of the oral administration of these supplements were compared in order to obtain valid data for recommendations for CaOx urolithiasis patients. A 10 mmol supplement of both ions decreased the oxalate absorption significantly, calcium being more than twice as effective.

Administration, Oral↗
PubMed1981

Effects of hydroxyproline and vitamin B-6 on oxalate synthesis in rats.

Relationships among dietary hydroxyproline (HP), vitamin B-6 and endogenous oxalate formation have been studied. In the absence of HP, urinary oxalate excretion was greatest among rats fed vitamin B-6-deficient diets. Supplementation of rat diets with 5.2% HP markedly increased the oxalate excretion of rats fed 0, 0.2 or 10 mg of vitamin B-6 per 100 g of diet, the increases being 2-, 19- and 15-fold respectively. The metabolism of several 14C-labeled oxalate precursors was altered in vitamin B-6-deficient rats. The feeding of HP and different levels of vitamin B-6 also altered their metabolism. The feeding of HP to vitamin B-6-deficient rats resulted in a decrease in the amount of 14C-oxalate formed from injected 14C-labeled glycine, glycolate or glyoxylate. In contrast, HP feeding to rats given 0.2 mg of vitamin B-6 per 100 g, resulted in a marked increase in oxalate formation from injected 14C-glycolate, as well as a decrease in respiratory 14CO2 from injected 14C-labeled glycolate and glyoxylate. HP feedings did not significantly alter the metabolism of these two injected compounds to oxalate or CO2 among rats fed the higher level of vitamin B-6, although some elevation of oxalate formation from glycolate was noted. HP feeding reduced the growth rates of all the rats, but growth depression was greatest in the vitamin B-6-deficient group.

Animals↗
PubMed1994

Oxalate, germin, and the extracellular matrix of higher plants.

The article assembles and elaborates evidence which indicates that an 'old' enzyme, oxalate oxidase, and an even 'older' substrate, calcium oxalate, have significant and previously uncontemplated roles in the biochemistry of the extracellular matrix (ECM) of higher plants. These possibilities emerged by chance, but not really by chance, when computerized comparisons of amino acid sequences inevitably led to the discovery that germin, long known to be a protein marker of the onset of growth in germinating wheat, and later known to be an ECM protein, is an oxalate oxidase [J. Biol. Chem. 268, 12239-12242 (1993)]. Dissolution of calcium oxalate, and germin-induced degradation of the resulting soluble oxalate, can release Ca2+ and H2O2, both of which are known to have central roles in the biochemistry of the ECM in higher plants. It is therefore timely to survey the implications of the recent finding that germin is an oxalate oxidase in the context of how oxalate may participate not only in the biochemistry of the ECM, but in the development of higher plants. The findings about oxalate, as a source of H2O2, are a complement to Varner's contemporaneous advocacy of a central role for H2O2 in the development, differentiation, vascularization and signaling processes of higher plants.

Calcium↗
PubMed1998

Oxalate, citrate, and sulfate concentration in human milk compared with formula preparations: influence on urinary anion excretion.

BACKGROUND: Nephrocalcinosis is not uncommon in preterm infants, and elevated urinary oxalate excretion is known to be one of the main risk factors. When oxalate excretion was found to be higher in formula-fed than in human milk-fed infants, the formulas' oxalate content was thought to be responsible. METHODS: The oxalate concentration in human milk (21 samples obtained during lactogenesis; 17 samples obtained during established lactation) and of 16 formula preparations was examined. Citrate and sulfate concentrations were also measured, because both anions influence urinary saturation. RESULTS: The mean (+/- SE) oxalate content of human milk increased approximately 27% from early lactogenesis (70.4 +/- 6.4 micromol/1) to established lactation (96.4 +/- 9.5 micromol/l; p < 0.05). The latter was not different from the mean oxalate concentration of formula (98.2 +/- 11.4 micromol/l), however a fourfold range of measurements was recorded in both groups. The mean citrate content of human milk increased only slightly after early lactogenesis (2.66 +/- 0.22 mmol/l), but remained significantly lower than in formula (3.34 +/- 0.23 mmol/l; p < 0.05). The mean sulfate concentration did not increase and was 13 times lower in human milk (52.1 +/- 9.5 micromol/l) than in formula (688.7 +/- 95.4 micromol/l; p < 0.0001). CONCLUSIONS: The higher oxalate excretion in formula-fed infants is not because of the milk's oxalate concentration. Urinary citrate and sulfate excretion may be influenced by their higher concentrations in formula preparations, which may be of clinical importance in the population that is at risk for development of nephrocalcinosis.

Anions↗
PubMed2003

Hepatic alanine-glyoxylate aminotransferase activity and oxalate metabolism in vitamin B6 deficient rats.

PURPOSE: Urinary oxalate has an important role in the formation of calcium oxalate stone and approximately 50% to 60% of urinary oxalate is derived from the endogenous metabolism of glyoxylate. Glyoxylate is enzymatically converted to glycine by alanine-glyoxylate aminotransferase in the liver and vitamin B6 has a key role as a coenzyme. Therefore, we evaluated hepatic alanine-glyoxylate aminotransferase activity and oxalate metabolism in vitamin B6 deficient rats. MATERIALS AND METHODS: A total of 12 male Wistar rats were fed a control or a vitamin B6 deficient diet. After 4 weeks creatinine, oxalate, glycolate, glycine and citrate in the urine, and alanine-glyoxylate aminotransferase activity and its mRNA level in the liver were measured. RESULTS: Urinary oxalate-to-creatinine and glycolate-to-creatinine ratios were significantly higher in vitamin B6 deficient rats than in control rats but urinary glycine-to-creatinine and citrate-to-creatinine ratios were significantly lower. Hepatic alanine-glyoxylate aminotransferase activity and its mRNA level were significantly lower in vitamin B6 deficient rats than in control rats. CONCLUSIONS: Vitamin B6 deficiency not only decreased alanine-glyoxylate aminotransferase activity, but also down-regulated alanine-glyoxylate aminotransferase gene expression by hepatocytes and led to hyperoxaluria and hyperglycolic aciduria secondary to impaired metabolism of oxalate precursors. Hyperoxaluria with hypocitruria may also contribute to calcium oxalate stone formation in vitamin B6 deficiency.

Animals↗
PubMed2005

The efficacy of dietary intervention on urinary risk factors for stone formation in recurrent calcium oxalate stone patients.

PURPOSE: Nutrition is suggested to be the major environmental risk factor in idiopathic calcium oxalate stone disease. The study was designed to evaluate the effect of dietary intervention on urinary risk factors for recurrence in calcium oxalate stone formers. MATERIALS AND METHODS: A total of 76 men and 31 women with idiopathic calcium oxalate stone disease collected 24-hour urine on their habitual, self-selected diets and after 7 days on a balanced standardized diet according to the recommendations for calcium oxalate stone formers. RESULTS: On the usual diet, a urine volume of less than 2.0 l per 24 hours was present in 57.9%, hypercalciuria in 25.2%, hypomagnesuria in 18.7%, hyperoxaluria in 14.0%, hyperuricosuria in 41.3% and hypocitraturia in 57.0% of patients. The frequency of metabolic abnormalities and the risk of calcium oxalate stone formation decreased significantly on the ingestion of the balanced diet, due to the significant increase in urinary volume, pH and citrate excretion and the significant decrease in urinary calcium and uric acid excretion. No change occurred in urinary oxalate and magnesium excretion. CONCLUSIONS: The evaluation of urinary risk profiles of the patients on their usual dietary habits revealed a high risk for calcium oxalate stone formation. A low fluid intake and an increased intake of protein and alcohol were identified as the most important dietary risk factors. The shift to a nutritionally balanced diet according to the recommendations for calcium oxalate stone formers significantly reduced the stone forming potential.

Adult↗
PubMed2005

Oxalate toxicity in cultured mouse inner medullary collecting duct cells.

PURPOSE: Oxalate, a metabolic end product and a major constituent of the majority of renal stones, has been shown to be toxic to renal epithelial cells of cortical origin. However, to our knowledge it is unknown whether inner medullary collecting duct (IMCD) cells, which are physiologically exposed to higher concentrations of oxalate, also behave in a similar manner. MATERIALS AND METHODS: A line of IMCD cells was exposed to oxalate (0.2 to 10 mM) for various time points. Trypan blue, and hematoxylin and eosin stains were used to assess cell morphology and membrane integrity. The production of reactive oxidative species was determined using the nitro blue tetrazolium reaction and crystal violet staining was used to measure cell density. RESULTS: Exposure of IMCD cells to oxalate produced time and concentration dependent changes in the light microscopic appearance of the cells. Long-term exposure to oxalate resulted in alterations in cell viability with net cell loss following exposure to concentrations of 2 mM and greater. Free radical production was time and concentration dependent. Crystal formation occurred in less than 1 hour and cells in proximity to crystals lost membrane integrity. Compared to IMCD cells LLC-PK1 and HK2 cells showed significant toxicity starting at lower oxalate concentrations (0.4 mM and above). CONCLUSIONS: To our knowledge the results provide the first direct demonstration of toxic effects of oxalate in IMCD cells, a line of renal epithelial cells of the inner medullary collecting duct, and suggest that cells lining the collecting duct are relatively resistant to oxalate toxicity.

Animals↗
PubMed2005

Study of a rat model for calcium oxalate crystal formation without severe renal damage in selected conditions.

BACKGROUND: Although nephrotoxic in high doses, ethylene glycol (EG) has been used with ammonium chloride (NH(4)Cl) or vitamin D(3) to study calcium oxalate stone formation in rat models. In the present study we used EG alone or with NH(4)Cl to study hyperoxaluria, crystaluria, and crystal attachment to renal epithelial cells in rats with minimal renal damage. METHODS: Six-week-old male Sprague-Dawley (SD) rats were given food and special drinking water. In experiment 1 the drinking water contained 1.0% NH(4)Cl plus four different concentrations of EG (0.8%, 0.4%, 0.2%, 0.1%). In experiment 2 the drinking water contained EG alone (0.8%, 0.4%, 0.2%, 0.1%). Urine was collected for 24 h before the rats were sacrificed. In experiment 1 the rats were sacrificed 5-13 days after starting the special water. In experiment 2 the rats were sacrificed 7-21 days after starting the special water. Bladder urine was also obtained. Blood and urine were tested for calcium, phosphorus, and creatinine. In addition, urine was tested for pH, oxalate and N-acetyl-beta-D glucosaminidase (NAG). Kidney sections were stained with hematoxylin-eosin, von Kossa and Pizzolato stain. Crystal morphology was determined using polarizing microscopy, and composition was determined using high-resolution X-ray powder diffraction. RESULTS: Experiment 1: Aggravation of renal function, an increase in urinary oxalate and NAG excretion, and crystals observed in the kidneys all correlated with EG concentration and length of drinking time. In bladder urine, calcium oxalate monohydrate (COM) crystals exceeded calcium oxalate dihydrate (COD) crystals. Experiment 2: Renal function remained unchanged. Oxalate excretion increased and NAG increased slightly. Crystals occurred only in the papillary tip region. Crystals in bladder urine were mostly COD. CONCLUSION: In the current rat model, calcium oxalate crystaluria could be induced without severe renal damage in selected cases. Either and/or both COM and COD might form and interact with kidney epithelium. We propose different experimental conditions to study the various phases of calcium oxalate stone formation in young male SD rats.

Acetylglucosaminidase↗
PubMed2005

Oxalate-degrading Providencia rettgeri isolated from human stools.

BACKGROUND: Oxalate-degrading bacteria are thought to metabolize intestinal oxalate and thus decrease the urinary excretion of oxalate by reducing its intestinal absorption. METHODS: We have isolated several novel oxalate-degrading bacteria from human stools. Oxalate degrading bacteria were investigated to characterize their protein profiles with antibodies against oxalyl-coenzyme A decarboxylase (65 kDa) and formyl-coenzyme A transferase (48 kDa) purified from Oxalobacter formigenes. RESULTS: One of these isolates was identified as Providencia rettgeri, which showed two proteins (65 kDa and 48 kDa) on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) that were not found in non-oxalate-degrading P. rettgeri. Antibodies reacted with the 65 and 48 kDa proteins from the P. rettgeri strain on Western blotting. An Oxalobacter formigenes formyl-coenzyme A transferase gene probe reacted with chromosomal DNA from P. rettgeri on Southern blotting under high stringency conditions, while an Oxalobacter formigenes oxalyl-coenzyme A decarboxylase gene probe did not react under the same conditions. CONCLUSIONS: The mechamism of oxalate degradation by P. rettgeri appears to be similar to that of Oxalobacter formigenes. This is the first report of a facultative oxalate-degrading organism that is one of the Enterobacteriaceae.

Blotting, Southern↗
PubMed1988

The role of magnesium in calcium oxalate urolithiasis.

The aim of this study was to evaluate the effect of magnesium on calcium oxalate crystal formation, both in physiological conditions and at slightly higher oxalate concentrations, using a mixed suspension mixed product removal crystallizer and scanning electron microscopy. True supersaturation ratios were calculated by allowing for complexation in solution. Magnesium inhibited the nucleation rate at all oxalate concentrations. It also inhibited the growth rate at oxalate concentrations of less than approximately 2.0 mmol/l but promoted the growth rate at higher concentrations. This suggests that, provided the oxalate concentration is sufficiently high, increase of magnesium concentration can increase the crystal growth rate. At physiological concentrations of oxalate, however, magnesium decreases both nucleation and growth rates. The SEM photographs showed that the predominant crystal was calcium oxalate trihydrate at low magnesium concentrations, with calcium oxalate dihydrate being observed in larger quantities at high magnesium concentrations.

Calcium Oxalate↗
PubMed1995

Effect of dietary intake on urinary oxalate excretion in calcium renal stone formers.

OBJECTIVE: To investigate the influence of dietary intake on urinary oxalate excretion in calcium renal-stone formers. PATIENTS AND METHODS: Dietary intake was monitored by using the dietary-record method in 60 idiopathic stone formers. The patients collected their urine for 24 h at home and their urinary oxalate excretion rate was determined. The relationship between the daily intake of various nutrients and urinary oxalate excretion was examined by both monovariate and multivariate analyses. RESULTS: By monovariate analysis, the intake of carbohydrate, total protein and fat were significantly correlated with urinary oxalate excretion, but the intake of calcium and body surface area were not. In addition, the intake of total protein was highly correlated with that of fat. By multivariate analysis, the intake of carbohydrate and fat were significantly related to urinary oxalate excretion, and the intake of calcium was inversely correlated with urinary oxalate excretion, but the intake of total protein showed no significant correlation. CONCLUSION: The intake of carbohydrate and fat was positively and the intake of calcium was inversely correlated with urinary oxalate excretion in stone formers and, taken together, these findings suggested that fat plays an important role in urinary oxalate excretion and that protein has a minimal effect.

Body Surface Area↗
PubMed2004

Fat malabsorption induced by gastrointestinal lipase inhibitor leads to an increase in urinary oxalate excretion.

BACKGROUND: Unabsorbed fat and bile acids may react with calcium in the intestinal lumen, limiting the amount of free calcium binding with oxalate and thereby raising intestinal oxalate absorption leading to hyperoxaluria. The aim of the present study was to determine whether orlistat (Xenical), a gastrointestinal lipase inhibitor, might increase urinary oxalate in an experimental rat model. METHODS: Thirty-nine male adult Wistar rats were fed a standard diet alone (controls) or supplemented with either 2% sodium oxalate (NaOx) or 3.2 mL of soy oil, or with both (NaOx + soy oil) for 4 weeks (diet period). Orlistat (16 mg/day) was added to the diet from the 5th to the 8th week (diet + orlistat period). Urinary oxalate (uOx), calcium (uCa), magnesium (uMg), and citrate (uCit) were determined and the ion-activity product of calcium oxalate [AP (CaOx) index(rat)] was estimated. RESULTS: Compared to baseline uOx significantly increased after diet + orlistat in controls (0.64 +/- 0.1 mg/24 hours vs. 0.56 +/-0.1 mg/24 hours), soy oil (0.80 +/- 0.3 mg/24 hours vs. 0.49 +/-0.2 mg/24 hours), and NaOx (2.48 +/- 0.8 mg/24 hours vs. 0.57 +/- 0.2 mg/24 hours), but the most marked increase occurred in NaOx + soy oil (3.87 +/- 0.7 mg/24 hours vs. 0.47 +/- 0.1 mg/24 hours). All groups except controls presented a significant reduction in uCa and uMg. Orlistat induced a significant increase in AP (CaOx) index(rat) compared, respectively, to baseline and to the diet period in NaOx (4.52 +/- 2.34 mg/24 hours vs. 0.94 +/- 0.86 and 1.53 +/- 0.93 mg/24 hours) and NaOx + soy oil (6.49 +/- 4.03 mg/24 hours vs. 0.54 +/- 0.17 and 1.76 +/- 1.32 mg/24 hours). CONCLUSION: These data suggest that the use of lipase inhibitors, especially under a diet rich in oxalate alone or associated with fat, leads to a significant and marked increase in urinary oxalate and a slight reduction in uCa and uMg that, taken together, resulted in an increase in AP (CaOx) index(rat), elevating the risk of stone formation.

Animals↗
PubMed1987

Microbial degradation of oxalate in the gastrointestinal tracts of rats.

Rates of oxalate degradation by mixed bacterial populations in cecal contents from wild rats ranged from 2.5 to 20.6 mumol/g (dry weight) per h. The oxalate-degrading activity in cecal contents from three strains of laboratory rats (Long-Evans, Wistar, and Sprague-Dawley) from four commercial breeders was generally lower, ranging from 1.8 to 3.5 mumol/g (dry weight) of cecal contents per h. This activity did not increase when diets were supplemented with oxalate. When Sprague-Dawley rats from a fifth commercial breeder were fed an oxalate diet, rates of oxalate degradation in cecal contents increased from 2.0 to 23.1 mumol/g (dry weight) per h. Obligately anaerobic, oxalate-degrading bacteria, similar to ruminal strains of Oxalobacter formigenes, were isolated from the latter group of laboratory rats and from wild rats. Viable counts of these bacteria were as high as 10(8)/g (dry weight) of cecal contents, which was less than 0.1% of the total viable population. This report presents the first evidence for the presence of anaerobic oxalate-degrading bacteria in the cecal contents of rats and represents the first direct measurement of the concentration of these bacteria in the large bowel of monogastric animals. We propose that methods used for the maintenance of most commercial rat colonies often preclude the intestinal colonization of laboratory rats with anaerobic oxalate-degrading bacteria.

Animals↗