Deamination of methylamine and aminoacetone increases aldehydes and oxidative stress in rats

Abstract

Semicarbazide-sensitive amine oxidase (SSAO)-mediated deamination of methylamine and aminoacetone in vitro produces carbonyl compounds, such as formaldehyde and methylglyoxal, which have been proposed to be cytotoxic and may be responsible for some pathological conditions. An HPLC procedure was developed to assess different aldehydes, which were derivatized with 2,4-dinitrophenylhydrazine (DNPH). We have demonstrated in vivo deamination of methylamine and aminoacetone by examining the excretion of formaldehyde and methylglyoxal, respectively, in rats. Following chronic administration of methylamine, the urinary level of malondialdehyde (MDA), an end product of lipid peroxidation, was also found to be substantially increased. A selective SSAO inhibitor blocked the increase of MDA. The results support the idea that increased SSAO-mediated deamination of methylamine and aminoacetone can be a potential cytotoxic risk factor.