Elevated norharman plasma levels in alcoholic patients and controls resulting from tobacco smoking

Breyer-Pfaff, U.; Wiatr, Gerlinde; Stevens, Ines; Gaertner, H. J.; Mundle, Götz; Mann, Karl

doi:10.1016/0024-3205(96)00112-9

Cited by 62 publications

(41 citation statements)

References 24 publications

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“…Tobacco and tobacco smoke are known to contain a number of compounds, among which monoamine oxidase inhibitors (MAOIs) have been the focus of special interest (Poindexter and Carpenter, 1962;Breyer-Pfaff et al, 1996;Rommelspacher et al, 2002). Many authors have found that tobacco smokers, when compared to nonsmokers, have MAO-A and -B activities that are reduced by up to 40% (Oreland et al, 1981;Yu and Boulton, 1987;Berlin et al, 1995;Fowler et al, 1996a, b).…”

Section: Introductionmentioning

confidence: 99%

Monoamine Oxidase Inhibitors Allow Locomotor and Rewarding Responses to Nicotine

Villegier

Salomon

Granon

et al. 2005

Neuropsychopharmacol

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Although nicotine is generally considered to be the main compound responsible for the addictive properties of tobacco, experimental data indicate that nicotine does not exhibit all the characteristics of other abused substances, such as psychostimulants and opiates. For example, nicotine is only a weak locomotor enhancer in rats and generally fails to induce a locomotor response in mice. This observation contradicts the general consensus that all drugs of abuse release dopamine in the nucleus accumbens, a subcortical structure, and thus increase locomotor activity in rodents. Because tobacco smoke contains monoamine oxidase inhibitors (MAOIs) and decreases MAO activity in smokers, we have combined MAOIs with nicotine to determine whether it is possible to obtain a locomotor response to nicotine in C57Bl6 mice. Among 15 individual or combined MAOIs, including harmane, norharmane, moclobemide, selegiline, pargyline, clorgyline, tranylcypromine and phenelzine, only irreversible inhibitors of both MAO-A and -B (tranylcypromine, phenelzine, and clorgyline + selegiline) allowed a locomotor response to nicotine. The locomotor stimulant interaction of tranylcypromine and nicotine was absent in b2-nicotinic acetylcholine receptor subunit knockout mice. Finally, it was found that, whereas naïve rats did not readily selfadminister nicotine (10 mg/kg/injection), a robust self-administration of nicotine occurred when animals were pretreated with tranylcypromine (3 mg/kg). Our data suggest that MAOIs contained in tobacco and tobacco smoke act in synergy with nicotine to enhance its rewarding effects.

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Section: Introductionmentioning

confidence: 99%

Monoamine Oxidase Inhibitors Allow Locomotor and Rewarding Responses to Nicotine

Villegier

Salomon

Granon

et al. 2005

Neuropsychopharmacol

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“…Actually, tobacco and tobacco smoke contain monoamine oxidases inhibitors (MAOIs) (Poindexter and Carpenter, 1962;Breyer-Pfaff et al, 1996;Rommelspacher et al, 2002). A few years ago, we showed that MAOI pretreatment allows the maintenance of behavioral sensitization to nicotine in rats (Villégier et al, 2003), thus suggesting a role of MAOIs in the addictive properties of tobacco.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Monoamine Oxidases Desensitizes 5-HT_1AAutoreceptors and Allows Nicotine to Induce a Neurochemical and Behavioral Sensitization

Lanteri

Vallejo²,

Salomon³

et al. 2009

J. Neurosci.

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Although nicotine is generally considered to be the main compound responsible for addictive properties of tobacco, experimental data indicate that nicotine does not exhibit all the characteristics of other substances of abuse. We recently showed that a pretreatment with mixed irreversible monoamine oxidases inhibitors (MAOIs), such as tranylcypromine, triggers a locomotor response to nicotine in mice and allows maintenance of behavioral sensitization to nicotine in rats. Moreover, we showed by microdialysis in mice that behavioral sensitization induced by compounds belonging to main groups of drugs of abuse, such as amphetamine, cocaine, morphine, or alcohol, was underlain by sensitization of noradrenergic and serotonergic neurons. Here, this neurochemical sensitization was tested after nicotine, tranylcypromine, or a mixture of both compounds. Data indicate that, whereas neither repeated nicotine nor repeated tranylcypromine alone has any effect by itself, a repeated treatment with a mixture of nicotine and tranylcypromine induces both behavioral sensitization and sensitization of noradrenergic and serotonergic neurons.

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“…In addition to alcoholic beverages, cigarette smoke may be the source of THH and its structural relatives because they are contained in the mainstream and sidestream [27]. Their plasma concentrations are remarkably increased by alcoholic beverage ingestion and also possibly by tobacco smoking [1].…”

Section: Discussionmentioning

confidence: 99%

Drinking-Related Tetrahydroharmans Counteract the Membrane Effects of Local Anesthetic Lidocaine

Tsuchiya

Mizogami²

2014

J Drug Alcohol Res

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There is a general consensus in dentistry that successful local anesthesia is frequently difficult in habitual drinkers and alcoholic patients. Neuro-active tetrahydroharmans increase in human body fluids and tissues by consuming alcoholic beverages. To understand such reduced anesthetic efficacy by the drug interaction hypothesis, we studied the influences of drinking-related tetrahydroharmans on membrane fluidization as one of local anesthetic mechanisms. Liposomal membranes prepared with phosphatidylcholine and cholesterol were treated with lidocaine and different tetrahydroharmans separately and in combination, followed by measuring fluorescence polarization to determine their induced changes in membrane fluidity. In contrast to 0.1-2 mg/mL lidocaine, tetrahydroharmans decreased the fluidity of membrane preparations at ∼ 25 μg/mL with the potency being 1,2,3,4-tetrahydroharman 1,2,3,4-tetrahydronorharman. 1,2,3,4-Tetrahydroharman counteracted the membrane-fluidizing effects of 1 mg/mL lidocaine at physiologically relevant 0.25-2.5 ng/mL, whereas neither its 6-hydroxyl nor 7-hydroxyl metabolite did at 25-200 ng/mL. Such counteraction at a membrane lipid level may be responsible for the reduction of local anesthetic efficacy in drinkers because 1,2,3,4-tetrahydroharman increases in vivo by ingesting alcoholic beverages.

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Elevated norharman plasma levels in alcoholic patients and controls resulting from tobacco smoking

Cited by 62 publications

References 24 publications

Monoamine Oxidase Inhibitors Allow Locomotor and Rewarding Responses to Nicotine

Monoamine Oxidase Inhibitors Allow Locomotor and Rewarding Responses to Nicotine

Inhibition of Monoamine Oxidases Desensitizes 5-HT_1AAutoreceptors and Allows Nicotine to Induce a Neurochemical and Behavioral Sensitization

Drinking-Related Tetrahydroharmans Counteract the Membrane Effects of Local Anesthetic Lidocaine

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Elevated norharman plasma levels in alcoholic patients and controls resulting from tobacco smoking

Cited by 62 publications

References 24 publications

Monoamine Oxidase Inhibitors Allow Locomotor and Rewarding Responses to Nicotine

Monoamine Oxidase Inhibitors Allow Locomotor and Rewarding Responses to Nicotine

Inhibition of Monoamine Oxidases Desensitizes 5-HT1AAutoreceptors and Allows Nicotine to Induce a Neurochemical and Behavioral Sensitization

Drinking-Related Tetrahydroharmans Counteract the Membrane Effects of Local Anesthetic Lidocaine

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Inhibition of Monoamine Oxidases Desensitizes 5-HT_1AAutoreceptors and Allows Nicotine to Induce a Neurochemical and Behavioral Sensitization