title: Low monoamine oxidase B in peripheral organs in smokers.
abstract: One of the major mechanisms for terminating the actions of catecholamines and vasoactive dietary amines is oxidation by monoamine oxidase (MAO). Smokers have been shown to have reduced levels of brain MAO, leading to speculation that MAO inhibition by tobacco smoke may underlie some of the behavioral and epidemiological features of smoking. Because smoking exposes peripheral organs as well as the brain to MAO-inhibitory compounds, we questioned whether smokers would also have reduced MAO levels in peripheral organs. Here we compared MAO B in peripheral organs in nonsmokers and smokers by using positron emission tomography and serial scans with the MAO B-specific radiotracers,l-[11C]deprenyl and deuterium-substituted l-[11C]deprenyl (l-[11C]deprenyl-D2). Binding specificity was assessed by using the deuterium isotope effect. We found that smokers have significantly reduced MAO B in peripheral organs, particularly in the heart, lungs, and kidneys, when compared with nonsmokers. Reductions ranged from 33% to 46%. Because MAO B breaks down catecholamines and other physiologically active amines, including those released by nicotine, its inhibition may alter sympathetic tone as well as central neurotransmitter activity, which could contribute to the medical consequences of smoking. In addition, although most of the emphases on the carcinogenic properties of smoke have been placed on the lungs and the upper airways, this finding highlights the fact that multiple organs in the body are also exposed to pharmacologically significant quantities of chemical compounds in tobacco smoke.
authors.affiliation: Chemistry Department and Medical Department, Brookhaven National Laboratory, Upton, NY 11973, USA. fowler@bnl.gov
authors.forename: Joanna S
authors.initials: JS
authors.lastname: Fowler
authors.forename: Jean
authors.initials: J
authors.lastname: Logan
authors.forename: Gene-Jack
authors.initials: GJ
authors.lastname: Wang
authors.forename: Nora D
authors.initials: ND
authors.lastname: Volkow
authors.forename: Frank
authors.initials: F
authors.lastname: Telang
authors.forename: Wei
authors.initials: W
authors.lastname: Zhu
authors.forename: Dinko
authors.initials: D
authors.lastname: Franceschi
authors.forename: Naomi
authors.initials: N
authors.lastname: Pappas
authors.forename: Richard
authors.initials: R
authors.lastname: Ferrieri
authors.forename: Colleen
authors.initials: C
authors.lastname: Shea
authors.forename: Victor
authors.initials: V
authors.lastname: Garza
authors.forename: Youwen
authors.initials: Y
authors.lastname: Xu
authors.forename: David
authors.initials: D
authors.lastname: Schlyer
authors.forename: S John
authors.initials: SJ
authors.lastname: Gatley
authors.forename: Yu-Shin
authors.initials: YS
authors.lastname: Ding
authors.forename: David
authors.initials: D
authors.lastname: Alexoff
authors.forename: Donald
authors.initials: D
authors.lastname: Warner
authors.forename: Noelwah
authors.initials: N
authors.lastname: Netusil
authors.forename: Pauline
authors.initials: P
authors.lastname: Carter
authors.forename: Millard
authors.initials: M
authors.lastname: Jayne
authors.forename: Payton
authors.initials: P
authors.lastname: King
authors.forename: Paul
authors.initials: P
authors.lastname: Vaska
mesh_terms: D006801:Humans; D008995:Monoamine Oxidase / Q000378:metabolism*; D008996:Monoamine Oxidase Inhibitors / Q000493:pharmacokinetics; D012642:Selegiline / Q000493:pharmacokinetics; D012907:Smoking / Q000378:metabolism*; D014055:Tomography, Emission-Computed
chemical_list: D008996:Monoamine Oxidase Inhibitors; D012642:Selegiline; D008995:Monoamine Oxidase