Oxalic acid occurs extensively in nature and plays diverse roles, especially in pathological processes. Due to its highly oxidizing effects, hyperabsorption or abnormal synthesis of oxalate can cause serious acute disorders in mammals and can be lethal in extreme cases. Intestinal oxalate-degrading bacteria could therefore be pivotal in maintaining oxalate homeostasis and reducing the risk of kidney stone development. In this study, the oxalate-degrading activities of 14 bifidobacterial strains were measured by a capillary electrophoresis technique. The oxc gene, encoding oxalyl-coenzyme A (CoA) decarboxylase, a key enzyme in oxalate catabolism, was isolated by probing a genomic library of Bifidobacterium animalis subsp. lactis BI07, which was one of the most active strains in the preliminary screening. The genetic and transcriptional organization of oxc flanking regions was determined, unraveling the presence of two other independently transcribed open reading frames, potentially responsible for the ability of B. animalis subsp. lactis to degrade oxalate. pH-controlled batch fermentations revealed that acidic conditions were a prerequisite for a significant oxalate degradation rate, which dramatically increased in cells first adapted to subinhibitory concentrations of oxalate and then exposed to pH 4.5. Oxalate-preadapted cells also showed a strong induction of the genes potentially involved in oxalate catabolism, as demonstrated by a transcriptional analysis using quantitative real-time reverse transcription-PCR. These findings provide new insights into the characterization of oxalate-degrading probiotic bacteria and may support the use of B. animalis subsp. lactis as a promising adjunct for the prophylaxis and management of oxalate-related kidney disease.Oxalate is a normal end product of amino acid metabolism and must be excreted, predominantly via the kidney, to maintain homeostasis (22). Oxalate is also present in a wide range of foods and drinks, and the normal dietary intake is variable, ranging from 70 to 920 mg per day (23). Because of its highly oxidizing effects and the capability to combine with cations to form insoluble salts, this organic dicarboxylate is extremely toxic for most forms of life. In humans, oxalate can cause a variety of pathological disorders, including hyperoxaluria, urolithiasis, cardiomyopathy, and renal failure (29,41,59). Hyperoxaluria is the single strongest promoter of kidney stone formation, whose medical management represents a burden to the individual patient as well as the health care system (49). The lack of new medications and the continued poor compliance with drug therapy have led to a growing interest in dietary manipulation and novel therapies aimed at preventing recurrent stone formation. Unfortunately, an oxalate-free diet is difficult to achieve and would probably be deficient in essential nutrients. Hence, other approaches to reducing urinary oxalate for management of stone disease have been explored.The discovery of oxalate-degrading bacteria within the human ...
