Increase of formation of methylamine and formaldehyde in vivo after administration of nicotine and the potential cytotoxicity.

摘要: Methylamine is a constituent of cigarette smoke and the major end product nicotine metabolism. Smoking or can induce release adrenaline, which in turn deaminated by monoamine oxidase, also producing methylamine. We found that urinary level methylamine was significantly elevated following administration (25 mg/Kg, i.p.). Semicarbazide-sensitive amine oxidase (SSAO) inhibitors further increased excretion induced nicotine. Following L-(—)-[N-methyl-3H]nicotine long-lasting irreversible radioactive adducts were detected different mouse tissues such adduct formation could be blocked selective SSAO inhibitors. These are probably cross-linked oligoprotein complexes formaldehyde. The findings support idea enhance SSAO/methylamine-mediated increase formaldehyde oxidative stress this part contribute adverse effect health associated with smoking.