Origin of excess urinary nitrate in the rat.
The ability of intestinal microorganisms to N-oxidize nitrogenous compounds to nitrite or nitrate was evaluated both in vivo and in vitro. Nitrate balance studies with germ-free and conventional rats indicated that the host and not the microbial flora is responsible for excess urinary nitrate. In vitro studies showed that most intestinal microorganisms are not able to N-oxidize nitrogenous compounds to nitrite. Although the metabolic pathway for endogenous nitrate formation remains unknown, the capacity of the rats to N-oxidize acetohydroxamate and hydroxylamine to nitrate indicates that such compounds could be intermediates in nitrate synthesis.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001419:Bacteria / Q000378:metabolism*; D002175:Candida / Q000378:metabolism; D005260:Female; D005856:Germ-Free Life; D006877:Hydroxamic Acids / Q000378:metabolism; D019811:Hydroxylamine; D006898:Hydroxylamines / Q000378:metabolism; D007422:Intestines / Q000382:microbiology*; D008297:Male; D009566:Nitrates / Q000378:metabolism / Q000652:urine*; D009573:Nitrites / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains
D000596:Amino Acids; D006877:Hydroxamic Acids; D006898:Hydroxylamines; D009566:Nitrates; D009573:Nitrites; D019811:Hydroxylamine; C006358:acetohydroxamic acid