Oxygenated nitrogen species, for example, the protonated form of nitrous ac
id (H2ONO+), dinitrogentrioxide (N2O3), dinitrogentetroxide (N2O4), or pero
xynitrite (ONOO-), can react with amines to form molecular nitrogen. These
reactions can occur spontaneously with primary aliphatic amines or via cyto
chrome P450 catalysed reactions with secondary amines. in principle measure
ments of the excretion of the molecular nitrogen generated by these reactio
ns could be used as an index of the levels of oxygenated nitrogen compounds
acting as nitrosating agents. To test this idea, [N-15(2)]urea (3 mmol) wa
s administered orally to live patients infected with Helicobacter pylori (a
s diagnosed by the [C-13]urea breath test) and to four healthy volunteers.
All participants ingested 3-mmol sodium nitrate as a precursor for NA 5 min
before the ingestion of the nitrogen tracer. During the test the participa
nts breathed 100% oxygen to increase the sensitivity of detection of endoge
nous molecular nitrogen. After the administration of [N-15(2)]urea, the pat
ients with H. pylori showed significantly increased N-15 enrichments of exh
aled N-2, expressed as delta value (parts per thousand), compared with heal
thy volunteers (patients: 3.5 +/- 0.9 vs, volunteers: 1.3 +/- 0.4; p < .05)
. We speculate that the endogenous production of molecular nitrogen is a pr
otective process controlling the body NO and nitrite levels. The N-15 breat
h technique allows the noninvasive estimation of the body nitrosation and c
ould indicate the health risk, possibly the oxidative stress status, caused
by highly reactive oxygenated nitrogen species and carbenium ion intermedi
ates. (C) 1999 Elsevier Science inc.