Male Fischer 344 rats were dosed with 2-bromoethanamine hydrobromide (BEA, N = 6) or [1,2,2,-2H4]-bromoethanamine hydrobromide (BEA-d4, N = 6) at 150 mg/kg i.p. and urine was collected -24 to 0 hr pre-dose and at 0-2 hr, 2-4 hr, 4-8 hr and 8-12 hr post-dose (p.d.). Urine samples were analysed directly using 500 and 600 MHz 1H NMR and 92.1 MHz 2H NMR spectroscopy. The major observed effect of BEA treatment was the induction of transient elevations in urinary glutaric acid (GTA) and adipic acid (ADA) excretion lasting up to 24 hr p.d. Most of the GTA was excreted in the 0-8 hr p.d. with maximal rates of 100-120 microM/hr for each rat occurring between 4 and 8 hr p.d. in animals treated with BEA or BEA-d4. GTA and ADA were shown to be of endogenous origin as there was no detectable incorporation of the 2H label into either compound following treatment of rats with BEA-d4. Following BEA-treatment there was an initial decrease in the levels of urinary citrate, succinate, 2-oxoglutarate and trimethylamine-N-oxide. A subsequent recovery of citrate and succinate was noted following the onset of medullary nephropathy. The abnormal urinary metabolite profiles were similar to that observed in the urine of humans with glutaric aciduria type II (an inborn error of metabolism) caused by a lack of mitochondrial fatty acyl coenzyme A dehydrogenases indicating that BEA or its metabolites have similar metabolic consequences. The BEA metabolite aziridine was detected by 1H and 2H NMR spectroscopy of the urine 8 hr p.d. together with BEA itself and two novel metabolites 2-oxazolidone (OX) and 5-hydroxy-2-oxazolidone (HOX). The formation of OX requires the reaction of BEA with endogenous bicarbonate followed by a cyclisation reaction eliminating HBr. Dosing rats with authentic OX resulted in the excretion of HOX but did not cause glutaric or adipic aciduria indicating that either aziridine or BEA itself was responsible for the presumed defect in mitochondrial metabolism.