Biogenic amines oxidase

Serendipity has played a major role in the discovery of most classes of psychotropic drugs. For example, the observation that the first antidepressants, the tricyclic antidepressants and the monoamine oxidase inhibitors, impeded the reuptake of biogenic amines into brain slices, or inhibited their metabolism, following their acute administration to rats, provided the experimenter with a mechanism that could be easily investigated in vitro. Such methods led to the development of numerous antidepressants that differed in their potency, and to some extent in their side effects (for example, the selective serotonin reuptake inhibitors) but did little to further the development of novel antidepressants showing greater therapeutic efficacy. The accidental discovery of atypical antidepressants such as mianserin led to the broadening of the basis of the animal models... 

Amine oxidases catalyze the oxidative deamination of both xenobiotic and biogenic amines, and thus have many critical biological functions. Two distinct classes differ in the nature of their prosthetic groups [1]. The flavin-(FAD flavin adenine dinucleotide)-dependent amine oxidases include monoamine oxidases (MAO A and B) and polyamine oxidases. Amine oxidases not containing FAD, the so-called semicarbazide-sensitive amine oxidases (SSAO), include both plasma amine oxidases and tissue amine oxidases. These contain quinonoid structures as redox cofactors that are derived from posttranslationally modified tyrosine or tryptophan side chains, topaoquinone frequently playing this role [2]. 

Table 6.2.2 Typical CSF profiles of HVA, 5HIAA and 3-methyldopa (3-MD) for the inborn errors of metabolism associated with a disruption of biogenic amine metabolism. A downward-pointing arrow indicates that a particular metabolite is below the established reference range. An upward pointing arrow is indicative that a metabolite is above the established reference range. WR indicates that the concentration of the metabolite is likely to be within the reference range. AADC Aromatic amino acid decarboxylase, PNPO pyridox(am)ine-5 -phosphate oxidase...

Strong support for the biogenic amine theory of depression is provided by the powerful antidepressant effect of inhibitors of monoamine oxidase. An example is pargyline (Fig. 30-33), which forms a covalent... 

Draisci et al. [7] Biogenic amines putrescine, cadaverine, histamine, tyramine, spermidine, spermine, tryptamine Anchovies Diamine oxidase (DAO)/on a nylon-net membrane, using glutaraldehyde Platinum electrode/ +0.650V vs. Ag/AgCl ... 

Development of sexual behavior can be affected by neonatal pharmacological treatment with the monoamine oxidase inhibitor pargyline, the monoamine depletor reserpine as well as with the acetylcholine esterase inhibitor pyridostigmine. These results suggest that biogenic amines are involved in sexual differentiation of the brain (refs. 162, 163). Pargyline treatment from day 1 to 14 or day 15 to 28 resulted in earlier development of puberty in female rats and delayed appearance of puberty in male rats. Male sexual behavior was decreased in both sexes. Treatment with reserpine on days 1, 4, 7 and 10 delayed the manifestation of puberty in both sexes, and caused disturbed female ovarian cycles and decreased male mounting behavior. 

Biogenic amines in wine and fermented foods are formed primarily via the microbial decarboxylation of amino acids. Examples, such as histamine, tyramine, and phenylethylamine are toxic, especially in alcoholic beverages. Ethanol can inhibit the monoamino oxidase responsible for amine detoxification (Maynard and Schenker, 1996). Histamine can induce allergenic reactions in humans, such as rashes, edema, headaches, hypotension. Tyramine and phenylethylamine can cause hypertension and other symptoms related to the release of noradrenaline. 

Special interest has been focused on the presence of biogenic amines in food plants (45, 90, 360-362), since digestion of food products rich in, e.g., tyramine can induce physiological effects, especially in patients using monoamine oxidase inhibitors as antidepressants (see below). Concentrations of alkaloids reported in food plants are summarized in Table II. 

Inhibitors of monoamine oxidase-B (MAO ). Monoamine oxidase occurs in the form of two isozymes MAOa and MAOB. The corpus striatumis rich in MAOB. This isozyme can be inhibited by selegiline. Degradation of biogenic amines in peripheral organs is not affected because MAOa remains functional. 

The biological function of amine oxidases involves the oxidation of biogenic amines formed during normal biological processes. In mammals, the monoamine oxidases are involved in the control of the serotonin catecholamine ratios in the brain, which in turn influence sleep and EEG patterns, body temperature, and mental depression. Two groups of amine oxidases are involved in the oxidative deamination of naturally occurring amines as well as foreign compounds. 

In plants, aliphatic di- and polyamines have been implicated in many processes including rapid cell division, fruit development, stress response and senescence (Evans and Malmberg, 1989 Galston and Kaur-Sawhney, 1995). Amine oxidases catalyse the eatabolism of biogenic amines and hence could be involved in regulating sueh eellular processes. It is eonve-nient to separate discussion of the roles of the copper-containing idiamine... 

Normally, if a low concentration of biogenic amines is ingested, these are quickly detoxified in fhe human body by amine oxidases or through conjugation. Amine... 

In severe cyanide poisonings, autonomic shock due to the release of biogenic amines plays a role. The coronary arterial vasoconstriction, resulting in an increase in central venous pressure, leads to the observed shock-hke state that is not attributable to inhibition of cytochrome oxidase (Vick and Froehlich, 1985). In the liver CN is metabohzed by rhodanese to thiocyanate, which is excreted in the urine. 

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