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Monoamine oxidase functions

Mitochondrial monoamine oxidase, 1, 253 Mitomycin synthesis, 7, 658, 659 Mitomycin-A, 7, 93 Mitomycin-B, 7, 93 Mitomycin-C, 7, 93 as antitumor drug, 4, 374 Mixed function oxidases, 1, 224 Mobam... [Pg.703]

Therapeutic Function Antidepressant monoamine oxidase inhibitor Chemical Name 4-Pyridinecarboxylic acid 2-(1-methylethyl)hydrazide Common Name —... [Pg.837]

MDMA overdose as well as the concomitant consumption of selective serotonin reuptake inhibitors (SSRI) with other dmgs that exert serotoninergic effects (such as inhibitors of monoamine oxidase) can rapidly lead to the serotonin syndrome. Its symptoms, which are reversible upon cessation, of the drug include confusion, muscle rigidity in the lower limbs, and hyperthermia suggesting an acute reaction to serotonin overflow in the CNS. Blocking the function of SERT outside the brain causes side effects (e.g., nausea), which may be due to elevated 5HT however , impairment of transporter function is not equivalent to direct activation of 5HT recqrtors in causing adverse effects such as fibrosis and pulmonary hypertension. [Pg.841]

Ephedra (sea grape, ma-huang, yellow horse) ephedra sinica Relieves colds, improves respiratory function, headaches, diuretic effects 3heart rate, psychosis l hedra should only be used after consulting with the physician. Many restrictions apply and the herb can cause serious reactions. Do not use with cardiac glycosides, monoamine oxidase inhibitor halothane, guanethidine, (MAOIs) or oxytocin. Do not use with 3. John s wort or in weight loss formulas. [Pg.660]

CYP. cytochrome P450 isoenzyme HIV, human immunodeficiency vims INR, International Normalized Ratio LFTs, liver function tests MAOI, monoamine oxidase inhibitor PT, prothrombin time TCA, tricyclic antidepressant. [Pg.535]

BUN, blood urea nitrogen CBC, complete blood cell count CNS, central nervous system CYP, cytochrome P-450 isoenzyme LFT, liver function test MAO, monoamine oxidase QTc, Q-T interval corrected for heart rate SCr, serum creatinine TMP-SMX, trimethoprim-sulfamethoxazole. [Pg.1183]

Virtually all types of drug that have been shown to be effective in major depression exert profound effects on the functioning of the serotoninergic or noradrenergic systems, or both. Although some treatments have been shown to decrease the sensitivity of certain postsynaptic 5-HT and NE receptors, it is generally believed that it is an enhancement of neurotransmission in these systems that is responsible for the improvement of the core symptoms of depression. For instance, long-term administration of tricyclic antidepressants (TCAs) or monoamine oxidase inhibitors (MAOIs) decreases the density of (3-adrenoceptors and cortical 5-HT2 receptors (Blier and Abbott 2003). [Pg.435]

Villegier AS, Salomon L, et al (2006) Monoamine oxidase inhibitors allow locomotor and rewarding responses to nicotine. Neuropsychopharmacology 31(8) 1704-1713 von Ziegler NI, Schlumpf M, et al (1991) Prenatal nicotine exposure selectively affects perinatal forebrain aromatase activity and fetal adrenal function in male rats. Brain Res Dev Brain Res 62(1) 23-31... [Pg.294]

Figure 2.18. The major pathway leading to the synthesis and metabolism of 5-hydroxytryptamine (5-HT). Metabolism of tryptophan to tryptamine is a minor pathway which may be of functional importance following administration of a monoamine oxidase (MAO) inhibitor. Tryptamine is a trace amine. L-Aromatic amino acid decarboxylase is also known to decarboxylate dopa and therefore the term "L-aromatic amino acid decarboxylase" refers to both "dopa decarboxylase"... Figure 2.18. The major pathway leading to the synthesis and metabolism of 5-hydroxytryptamine (5-HT). Metabolism of tryptophan to tryptamine is a minor pathway which may be of functional importance following administration of a monoamine oxidase (MAO) inhibitor. Tryptamine is a trace amine. L-Aromatic amino acid decarboxylase is also known to decarboxylate dopa and therefore the term "L-aromatic amino acid decarboxylase" refers to both "dopa decarboxylase"...
Recently research has focused on the action of lithium on serotonergic function. Lithium has been shown to facilitate the uptake and synthesis of 5-HT, to enhance its release and to increase the transport of tryptophan into the nerve terminal, an effect which probably contributes to the increased 5-HT synthesis. The net effect of these changes is to produce postsynaptic receptor events, which might explain why lithium, in combination with tryptophan and a monoamine oxidase inhibitor or a 5-HT uptake inhibitor, is often effective in therapy-resistant depression. [Pg.203]

Serotonin mediates many central and peripheral physiological functions, including contraction of smooth muscle, vasoconstriction, food intake, sleep, pain perception, and memory, a consequence of it acting on several distinct receptor types. Although 5-HT may be metabolized by monoamine oxidase, platelets and neurons possess a high-affinity mechanism for reuptake of 5-HT. This mechanism may be inhibited by the widely prescribed antidepressant drugs termed selective serotonin re-uptake inhibitors (SSRl), e.g. fluoxetine (Prozac ), thereby increasing levels of 5-HT in the central nervous system. [Pg.446]

Binda, C., Mattevi, A. and Edmondson, D.E. (2002) Structure-function relationships in flavoenzyme-dependent amine oxidations. A comparison of polyamine oxidase and monoamine oxidase. The Journal of Biological Chemistry, 277, 23973-2397(>. [Pg.285]

Hamilton SP, Slager SL, Heiman GA, Haghighi F, Klein DF, Hodge SE, Weissman MM, Fyer AJ, Knowles JA (2000b) No genetic linkage or association between a functional promoter polymorphism in the monoamine oxidase-A gene and panic disorder. Mol Psychiatry 5 465-466... [Pg.174]


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See also in sourсe #XX -- [ Pg.296 ]




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