Genome Sequence of Strain OXCC13.

The lack of colonization in the human gut is generally acknowledged as a risk factor for kidney stone formation since this microorganism can play an important role in oxalate homeostasis. Here, we present the genome sequence of OXCC13, a human strain isolated from an individual residing in Germany.

Genome Sequence of Strain HC-1.

The lack of colonization of the human gut has been correlated with the formation of calcium oxalate kidney stones and also with the number of recurrent kidney stone episodes. Here, we present the genome sequence of HC-1, a human strain isolated from an individual residing in Iowa, USA.

Enteric oxalate elimination is induced and oxalate is normalized in a mouse model of primary hyperoxaluria following intestinal colonization with Oxalobacter.

Oxalobacter colonization of rat intestine was previously shown to promote enteric oxalate secretion and elimination, leading to significant reductions in urinary oxalate excretion (Hatch et al. Kidney Int 69: 691-698, 2006). The main goal of the present study, using a mouse model of primary hyperoxaluria type 1 (PH1), was to test the hypothesis that colonization of the mouse gut by Oxalobacter formigenes could enhance enteric oxalate secretion and effectively reduce the hyperoxaluria associated with this genetic disease.

Toxicity and metabolism of the conjugates of 3-nitropropanol and 3-nitropropionic acid in forages poisonous to livestock.

Glycosides of 3-nitro-1-propanol (nitropropanol) and glucose esters of 3-nitro-1-propanoic acid (nitropropionic acid) occur in many forages distributed throughout the world. Systemically, nitropropionic acid irreversibly inactivates succinate dehydrogenase, thereby blocking ATP formation. Nitropropanol is not toxic per se in mammals but is converted to nitropropionic acid by hepatic alcohol dehydrogenase.

Oxalobacter formigenes and its potential role in human health.

Oxalate degradation by the anaerobic bacterium Oxalobacter formigenes is important for human health, helping to prevent hyperoxaluria and disorders such as the development of kidney stones. Oxalate-degrading activity cannot be detected in the gut flora of some individuals, possibly because Oxalobacter is susceptible to commonly used antimicrobials. Here, clarithromycin, doxycycline, and some other antibiotics inhibited oxalate degradation by two human strains of O.