AHHH! You are kidding me right? Check the premise of the thread for study that "proves" smoking cigarettes has an MAOI in it. MAOIs are medications that have serious interaction effects with other drugs and foods. When a client is put on this mood-altering substance they have diet restrictions and the pairing with some drugs can be fatal.
An old abstract: Tobacco smoke, beta-carboline alkaloids, and reversible MAO inhibition
ABSTRACTMonoamine oxidase (MAO) is a mitochondrial outer-membrane flavoenzyme involved in brain and peripheral oxidative catabolism of neurotransmitters and xenobiotic amines, including neurotoxic amines, and a well-known target for antidepressant and neuroprotective drugs. Recently, positron emission tomography imaging has shown that smokers have a much lower activity of peripheral and brain MAO-A (30%) and -B (40%) isozymes compared to non-smokers. This MAO inhibition results from a pharmacological effect of smoke, but little is known about its mechanism. Working with mainstream smoke collected from commercial cigarettes we confirmed that cigarette smoke is a potent inhibitor of human MAO-A and -B isozymes. MAO inhibition was partly reversible, competitive for MAO-A, and a mixed-type inhibition for MAO-B. Two beta-carboline alkaloids, norharman (beta-carboline) and harman (1-methyl-beta-carboline), were identified by GC-MS, quantified, and isolated from the mainstream smoke by solid phase extraction and HPLC. Kinetics analysis revealed that beta-carbolines from cigarette smoke were competitive, reversible, and potent inhibitors of MAO enzymes. Norharman was an inhibitor of MAO-A (K(i)=1.2+/-0.18muM) and MAO-B (K(i)=1.12+/-0.19muM), and harman of MAO-A (K(i)=55.54+/-5.3nM). beta-Carboline alkaloids are psychopharmacologically active compounds that may occur endogenously in human tissues, including the brain. These results suggest that beta-carboline alkaloids from cigarette smoke acting as potent reversible inhibitors of MAO enzymes may contribute to the MAO-reduced activity produced by tobacco smoke in smokers. The presence of MAO inhibitors in smoke like beta-carbolines and others may help us to understand some of the purported neuropharmacological effects associated with smoking.
My Remarks: So, based on PET scans smokers have a 30% and 40% level of decrease in MAO that may have competative, interactional, and reversible effects. Two beta-carboline alkaloids, harman and norharman were isolated from mainstream smoke and offered as the source for the inhibitory effect on the MAO.
Let's analyze what that means...
Pet scans are a wonderful tool but unfortunately the images are still interpreted from what theory we use to guesstimate what the chemicals in our brains are doing. But they are cool...!
Since a smoker's petscan shows decreased MAO enzymes one would assume they are less depressed, not a bad thing. But smokers may also be biologically wired from birth to have decreased MAO activity. Their environment and inherent flexibility may also impact the brain chemistry. The scans are not demonstrating cause and effect.
Isolating two beta-carboline alkaloids, harman and norharman, from mainstream smoke to offer as the probable culprits of this action is quite interesting but funny. Thus, I suspect the premise. If the agonist of harman is norharman, then the effect is a canceling out...the authors refer to this as competing and reversible. The same thing happens with epinephrine and norepinephrine (adrenaline and noradrenaline).
The use of the terminolgy such as suggestive, may, purported, etc is indicative that this is a theory that requires more research. One should view these findings with cautioned interest in my opinion.
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