Catecholamine Metabolism: From Molecular Understanding to Clinical Diagnosis and Treatment

摘要: Publisher Summary Catecholamines are metabolized by multiple pathways involving oxidative deamination catalyzed monoamine oxidase (MAO), O-methylation catechol O-methyltransferase (COMT) and conjugation sulfotransferases or glucuronidases. Aldehyde reductase aldehyde dehydrogenase other enzymes that participate in sequence with MAO the production of respective glycol acid deaminated metabolites. Additionally, alcohol contributes to formation homovanillic vanillylmandelic (VMA), final end-products catecholamine metabolism. This multiplicity metabolic ensures redundancy mechanisms inactivation also leads a wide array The metabolism depend on compartmentalization catabolic among different cells tissues. is sole metabolizing enzyme present catecholaminergic neurons. metabolite norepinephrine, dihydroxyphenylglycol (DHPG), provides marker intraneuronal Differences tissues organs considered. VMA, end-product norepinephrine epinephrine predominant excreted urine, produced almost exclusively liver, mainly from metabolites DHPG 3-methoxy-4-hydroxyphenylglycol. Intraneuronal main determinant turnover; most this dependent leakage transmitter vesicular stores contribution re-uptake only becoming important increases exocytotic release. As illustrated chapter, studies provide an ideal contextural framework for bridging molecular biologic, genetic, neurochemical, psychological, clinical areas interest. chapter details deamination, catechol-O-methyltransferase, glucuronidases, sulphotransferases, systems. advances described section illustrate how area offers context basic research. It can be anticipated future investigation will continue conceptual mortar cementing together integrative understanding systems health disease.