Explanation: Monoamine oxidases (MAOs) are indeed classified under EC 1.4.3.4 and function by catalyzing the oxidative deamination of monoamines, which involves the removal of the amine group.

Explanation: The cellular localization of monoamine oxidases is primarily the outer membrane of mitochondria across various cell types.

Explanation: Historical accounts confirm that Mary Bernheim discovered the first MAO enzyme in 1928 in the liver, initially naming it tyramine oxidase.

Explanation: MAOs are classified within the flavin-containing amine oxidoreductases family, utilizing flavin adenine dinucleotide (FAD) as an essential cofactor for their enzymatic activity.

Explanation: Monoamine oxidases are critical for both the metabolic breakdown of dietary monoamines and the inactivation of endogenous monoamine neurotransmitters, thereby regulating their physiological concentrations.

Explanation: The catalytic process of MAOs involves oxidative deamination, wherein the FAD cofactor facilitates the oxidation of the monoamine substrate to an imine intermediate.

Explanation: The Chemical Abstracts Service (CAS) registry number for monoamine oxidase is 9001-66-5.

Explanation: The enzymatic reaction catalyzed by monoamine oxidase involves oxidative deamination, which necessitates molecular oxygen for the regeneration of the FAD cofactor from its reduced state.

Explanation: MAOs catalyze the oxidation, not reduction, of monoamines. The process is oxidative deamination, not reduction.

Explanation: MAOs are primarily membrane-bound, specifically located on the outer mitochondrial membrane, not free-floating in the cytoplasm.

Explanation: The first MAO enzyme was discovered by Mary Bernheim in 1928, but it was found in the liver, not the brain, and was initially named tyramine oxidase.

Explanation: MAOs are classified as oxidoreductases, not hydrolases, and critically require FAD as a cofactor for their enzymatic activity.

Explanation: MAOs function in the catabolism (breakdown) of monoamine neurotransmitters, not their synthesis.

Explanation: MAOs catalyze oxidative deamination, not reduction, and utilize FAD as a cofactor, not NADPH.

Explanation: While the nucleophilic model and hydride transfer are proposed mechanisms, there are other models, and strong supporting evidence for any single model is still debated.

Explanation: MAOs catalyze the oxidative deamination of monoamines, a process involving the removal of the amine group.

Explanation: Monoamine oxidases are predominantly localized to the outer mitochondrial membrane in most cell types.

Explanation: The first MAO enzyme was discovered by Mary Bernheim in 1928 and was initially named tyramine oxidase.

Explanation: Monoamine oxidases are classified as flavin-containing amine oxidoreductases due to their structure and reliance on FAD.

Explanation: MAOs perform a dual function: metabolizing dietary monoamines and inactivating endogenous monoamine neurotransmitters.

Explanation: In the catalytic mechanism, FAD oxidizes the monoamine substrate, leading to the formation of an imine intermediate.

Explanation: The CAS registry number for monoamine oxidase is 9001-66-5.

Explanation: Monoamine oxidase catalyzes oxidative deamination, a reaction where FAD oxidizes the substrate to an imine, generating FADH2.

Explanation: Humans possess two principal subtypes of monoamine oxidase: MAO-A and MAO-B, which exhibit distinct substrate specificities and tissue distributions.

Explanation: Within the central nervous system, both MAO-A and MAO-B are expressed in neuronal and astroglial cells.

Explanation: Extracerebral distribution of MAO-A includes significant presence in the liver, pulmonary vascular endothelium, gastrointestinal tract, and placenta.

Explanation: Beyond the central nervous system, MAO-B exhibits a predominant localization in blood platelets.

Explanation: Developmental studies indicate that MAO-B is largely undetectable in the infant brain, whereas MAO-A levels are substantial, reaching approximately 80% of adult concentrations at birth.

Explanation: Neuroanatomical studies reveal that the striatum and globus pallidus are characterized by substantial MAO-B presence and minimal MAO-A.

Explanation: Research suggests a correlation between MAO-A concentrations and serotonergic pathways, while MAO-B levels are associated with noradrenergic systems.

Explanation: MAO-A exhibits a primary role in the metabolic breakdown of key monoamines, including serotonin, norepinephrine, and epinephrine.

Explanation: Phenethylamine and benzylamine are recognized as primary substrates for the MAO-B enzyme.

Explanation: Dopamine, tyramine, and tryptamine are substrates for both MAO-A and MAO-B, with MAO-B's contribution to dopamine degradation being considered less significant.

Explanation: MAOs metabolize not only primary neurotransmitters but also endogenous compounds such as telemethylhistamine and N-acetylputrescine.

Explanation: Exogenous substances, including pharmaceuticals like phenylephrine and dimethyltryptamine (DMT), are recognized substrates for MAO enzymes.

Explanation: The oxidative deamination of serotonin by MAO yields 5-hydroxyindoleacetaldehyde.

Explanation: This statement incorrectly assigns substrate specificities. MAO-A primarily metabolizes serotonin, norepinephrine, and epinephrine, while MAO-B preferentially metabolizes phenethylamine and benzylamine.

Explanation: Outside the CNS, MAO-A is predominantly found in the liver and placenta, whereas MAO-B is primarily located in blood platelets.

Explanation: The striatum and globus pallidus are characterized by significant amounts of MAO-B and very little MAO-A, contrary to the statement.

Explanation: MAO-B is predominantly found in blood platelets outside the CNS, while MAO-A is found in the liver, gastrointestinal tract, and placenta.

Explanation: Infant brains have nearly undetectable MAO-B levels, while MAO-A levels are approximately 80% of adult levels at birth, which is the opposite of the statement.

Explanation: The cortex generally has high MAO-A levels, while the striatum and globus pallidus have high MAO-B levels with minimal MAO-A.

Explanation: Studies indicate MAO-A concentrations correlate with serotonergic neurotransmission, while MAO-B levels correlate with norepinephrine, not dopaminergic or serotonergic respectively.

Explanation: Dopamine, tyramine, and tryptamine are metabolized by both MAO-A and MAO-B, not exclusively by MAO-B.

Explanation: The oxidative deamination of serotonin by MAO yields 5-hydroxyindoleacetaldehyde, not DOPAL, which is derived from dopamine.

Explanation: MAO-A is primarily responsible for the catabolism of serotonin, norepinephrine, and epinephrine.

Explanation: MAO-B primarily metabolizes phenethylamine and benzylamine.

Explanation: Dopamine, tyramine, and tryptamine are substrates for both MAO-A and MAO-B.

Explanation: Both MAO-A and MAO-B are distributed within neurons and astroglia throughout the central nervous system.

Explanation: Beyond the CNS, MAO-A is predominantly located in the liver, pulmonary vascular endothelium, gastrointestinal tract, and placenta.

Explanation: Outside the CNS, MAO-B is predominantly found in blood platelets.

Explanation: In the infant brain, MAO-A levels are substantial (approx. 80% of adult levels), while MAO-B is nearly undetectable.

Explanation: The hypothalamus and the hippocampal uncus are brain regions characterized by very high concentrations of both MAO-A and MAO-B.

Explanation: Studies suggest that MAO-B levels in the brain correlate with norepinephrine systems, while MAO-A correlates with serotonergic systems.

Explanation: Telemethylhistamine is an endogenous compound, besides major neurotransmitters, that serves as a substrate for MAO enzymes.

Explanation: Sumatriptan is cited as an example of an exogenous drug that acts as a substrate for MAO enzymes.

Explanation: The oxidative deamination of dopamine by MAO yields 3,4-dihydroxyphenylacetaldehyde (DOPAL).

Explanation: Phenethylamine is primarily metabolized by MAO-B, not MAO-A. Serotonin, norepinephrine, and epinephrine are primary substrates for MAO-A.

Explanation: Serotonin is primarily metabolized by MAO-A. Phenethylamine, benzylamine, and dopamine are primary substrates for MAO-B.

Explanation: Blood platelets are a primary location for MAO-B outside the CNS. MAO-A is predominantly found in the liver, pulmonary vascular endothelium, gastrointestinal tract, and placenta.

Explanation: MAO-A and MAO-B exhibit significant structural homology, sharing approximately 70% of their amino acid sequence, and feature predominantly hydrophobic substrate binding pockets.

Explanation: The genes responsible for MAO-A and MAO-B are located in close proximity on the short arm of the human X chromosome.

Explanation: Brunner syndrome is a genetic condition linked to rare mutations affecting the MAO-A gene.

Explanation: Longitudinal studies, such as the Dunedin cohort study, have indicated a potential gene-environment interaction, where maltreated children with a low-activity MAO-A promoter polymorphism show an increased propensity for antisocial conduct disorders.

Explanation: Certain variants of the MAO-A gene have been associated with personality traits, including a predisposition towards novelty seeking.

Explanation: The genetic loci for MAO-A and MAO-B are situated on the X chromosome, specifically within the p11.4-p11.3 region of the short arm.

Explanation: Specific tyrosine residues, such as Tyr398 and Tyr435 in MAO-B, are proposed to play a critical role in substrate orientation within the enzyme's active site.

Explanation: Evidence suggests that a low-activity variant of the MAO-A gene promoter may increase the risk for adolescent conduct disorder in individuals who have experienced childhood maltreatment.

Explanation: While the genes for MAO-A and MAO-B share approximately 70% sequence similarity, they are located on the X chromosome, not chromosome 1.

Explanation: MAO-A and MAO-B share approximately 70% of their structure and possess largely similar, albeit distinct, substrate binding pockets.

Explanation: MAO-A and MAO-B exhibit significant structural similarity, sharing approximately 70% of their amino acid sequence.

Explanation: The genes encoding MAO-A and MAO-B are located on the short arm of the X chromosome.

Explanation: Brunner syndrome is a rare genetic disorder linked to mutations in the MAO-A gene.

Explanation: The Dunedin cohort study indicated that childhood maltreatment combined with a low-activity MAO-A gene promoter polymorphism increased the likelihood of developing antisocial conduct disorders.

Explanation: The proposed mechanism suggests that reduced MAO-A activity impairs norepinephrine degradation, potentially leading to heightened sympathetic responses and contributing to antisocial behavior.

Explanation: A criticism of the MAO-A genotype-maltreatment link is that genetic predispositions to antisocial behavior might be inherited from parents through genes other than MAO-A.

Explanation: The official gene symbol for monoamine oxidase A is MAOA.

Explanation: Tyrosine residues within the MAO binding pocket are hypothesized to be crucial for correctly orienting the substrate molecules for catalysis.

Explanation: A key criticism is that genetic predispositions to antisocial behavior may be inherited from abusive parents via genes other than the MAO-A variant.

Explanation: A criticism of the MAO-A genotype-maltreatment link is that genetic predispositions to antisocial behavior may be inherited from abusive parents via genes other than the MAO-A variant.

Explanation: Dysregulation of MAO activity is implicated in the pathophysiology of various neurological and psychiatric conditions, including schizophrenia, depression, and migraines.

Explanation: Monoamine oxidase inhibitors (MAOIs) are frequently employed as later-line treatments for depression owing to the risk of severe adverse events, such as hypertensive crisis, resulting from interactions with tyramine-rich foods and certain medications.

Explanation: MAO-A inhibitors are primarily utilized for their antidepressant and anxiolytic properties.

Explanation: MAO-B inhibitors find application in the therapeutic management of neurodegenerative conditions such as Alzheimer's disease and Parkinson's disease.

Explanation: The pathogenesis of sleep disturbances in African trypanosomiasis is linked to the parasite's interference with host MAO activity, specifically within the orexin system.

Explanation: The relationship is reversed: excessive levels of catecholamines can precipitate a hypertensive crisis, whereas excessive serotonin is associated with serotonin syndrome.

Explanation: The 'cheese effect' describes a hypertensive crisis resulting from MAOIs interacting with tyramine-rich foods, which *allows* tyramine levels to rise dangerously, rather than preventing a rise.

Explanation: MAOIs require careful management due to significant risks of adverse effects, particularly hypertensive crisis, when combined with tyramine-rich foods (like aged cheeses) and certain medications.

Explanation: MAOIs are generally not considered first-line treatments for depression due to their potential for significant side effects and drug/food interactions, often making them a last-line option.

Explanation: MAO-A inhibitors are primarily used as antidepressants and anti-anxiety agents. MAO-B inhibitors are typically used for conditions like Parkinson's and Alzheimer's disease.

Explanation: African trypanosomiasis disrupts sleep by interfering with MAO activity within the host's orexin system, not by directly destroying the enzymes.

Explanation: The 'cheese effect' accurately describes the hypertensive crisis resulting from concurrent MAOI use and tyramine-rich foods, due to the unchecked rise in tyramine levels.

Explanation: Excessive levels of catecholamines are associated with hypertensive crisis, while excessive serotonin levels lead to serotonin syndrome.

Explanation: Dysregulation of MAO activity is implicated in the development or exacerbation of disorders such as schizophrenia and depression.

Explanation: MAOIs are often reserved for last-line treatment due to the potential for severe adverse effects, including hypertensive crisis, arising from interactions with specific foods and medications.

Explanation: MAO-A inhibitors are primarily utilized for their efficacy as antidepressant and anti-anxiety agents.

Explanation: African trypanosomiasis is linked to MAO activity through the parasite's interference with the host's orexin system, contributing to sleep disturbances.

Explanation: Excessive levels of catecholamines, such as norepinephrine and epinephrine, are known to precipitate a hypertensive crisis.

Explanation: The 'cheese effect' describes a potentially dangerous hypertensive crisis that can occur when MAOIs interact with tyramine found in aged cheeses and other foods.

Explanation: MAOIs function by inhibiting MAO enzymes, thereby preventing the breakdown of monoamine neurotransmitters and increasing their availability in the synaptic cleft.

Explanation: Excessive serotonin levels in the body can lead to a condition known as serotonin syndrome.

Explanation: Emerging research indicates that MAO-B in the rodent striatum may play a role in GABA synthesis from putrescine, potentially modulating dopaminergic neuronal activity.

Explanation: Species-specific differences exist in dopamine metabolism; rats primarily utilize MAO-A, while humans and vervet monkeys rely predominantly on MAO-B for this process.

Explanation: Genetic studies in mice reveal that the absence of functional MAO-A or MAO-B is associated with autistic-like behaviors and heightened stress reactivity.

Explanation: The mechanism of action for certain insecticides, such as chlordimeform, involves the inhibition of MAO enzymes within insect physiology.

Explanation: Age-related changes include an observed increase in MAO-B activity within the brain and pineal gland across mammalian species.

Explanation: Recent findings suggest that MAO-B in astrocytes contributes to GABA synthesis from putrescine, playing a role in neuronal regulation.

Explanation: The emerging understanding of MAO-B's involvement in GABA synthesis suggests that MAO-B inhibitors may have broader implications for Parkinson's disease treatment than previously recognized.

Explanation: The age-related rise in MAO-B activity is hypothesized to be a factor in the decline of monoamine concentrations observed in aging populations.

Explanation: Contrary to the statement, in vervet monkeys (and humans), dopamine is primarily deaminated by MAO-B, not MAO-A. Rats primarily use MAO-A for dopamine deamination.

Explanation: Recent research suggests MAO-B in the rodent striatum primarily synthesizes GABA from putrescine, rather than degrading dopamine or playing a role in its synthesis.

Explanation: The primary enzyme responsible for dopamine deamination differs by species: rats utilize MAO-A, while humans and vervet monkeys utilize MAO-B.

Explanation: Mice lacking functional MAO-A or MAO-B exhibit autistic-like traits and an increased response to stress, not enhanced cognitive function or reduced stress responses.

Explanation: MAO-B facilitates the synthesis of GABA from putrescine, not dopamine, within astrocytes.

Explanation: Recent research indicates that MAO-B in the rodent striatum may synthesize GABA from putrescine, thereby inhibiting dopaminergic neurons, suggesting a role beyond traditional monoamine degradation.

Explanation: Species differences are notable: rats primarily deaminate dopamine via MAO-A, whereas humans and vervet monkeys utilize MAO-B for this function.

Explanation: Mice genetically engineered to lack functional MAO-A or MAO-B exhibit behavioral phenotypes including autistic-like traits and heightened stress reactivity.

Explanation: MAO-B activity increases with aging, which may contribute to the observed decrease in monoamine levels in older individuals.

Explanation: Recent research indicates that MAO-B in astrocytes synthesizes GABA from putrescine, contributing to neuronal regulation.

Explanation: The discovery of MAO-B's role in GABA synthesis implies that MAO-B inhibitors may exert broader therapeutic effects in conditions like Parkinson's disease than initially understood.

Explanation: The increase in MAO-B activity during aging may contribute to the decline in monoamine levels commonly observed in older individuals.

Explanation: Recent research suggests MAO-B in the rodent striatum primarily synthesizes GABA from putrescine, a role distinct from traditional monoamine degradation.