MAO is mainly located in the outer membrane of mitochondria of presynaptic nerve terminals, where oxidative deamination of norepinephrine, epinephrine, and serotonin by MAO inactivates these neurotransmitters and abrogates the neural stimulus. Both MAO-A and MAO-B are expressed in several human tissues, with the highest concentrations evident in liver, followed by myocardium, renal cortex, and intestine.57 MAO-A is selectively expressed in the placenta while MAO-B is selectively expressed in blood platelets.58 Intestinal MAO is implicated in the breakdown of dietary amines, notably the indirectly acting sympathomimetic tyramine, which is present in high concentrations in aged cheeses and red wine. Normally, tyramine is metabolized by intestinal MAO before it enters systemic circulation. When MAOIs, like isoniazid and tranylcypromine and foods high in tyramine are taken concurrently, large amounts of dietary tyramine can reach the systemic circulation and precipitate a hypertensive crisis.59
Limited studies on the ontogenic development of MAO have been performed and most available data deal with developmental aspects of MAO in the human brain.58 In the fetal brain, lung, aorta, and digestive tract, MAO-A activity is detected earlier than MAO-B, and in the fetal brain the levels of MAO-A are significantly higher than MAO-B (Table 4). Interestingly, during aging, in which a general decrease in most enzymatic activity is observed, MAO-B content and activity appear to increase, due perhaps to astroglial proliferation and the associated increased need to metabolize the resulting biogenic amines.58
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