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Biogenic Amines in Plant Food
Published in Akula Ramakrishna, Victoria V. Roshchina, Neurotransmitters in Plants, 2018
Kamil Ekici, Abdullah Khalid Omer
Polyamines are essential compounds for growth and development in plants. Since only polyamines spermidine and spermine share a common precursor S-adenosylmethionine (SAM) with ethylene, they demonstrated competitive effects on functions in fruit development and ripening in many plants. Polyamines are essential compounds for growth and development in plants. Since polyamines only spermidine and spermine share a common precursor S-adenosylmethionine (SAM) with ethylene, they demonstrated competitive effects on functions in fruit development and ripening in many plants. In higher plants generally, the polyamines are found in both free and conjugated forms its endogenous levels depend on the external conditions of light and temperature. Especially in reproductive organs and seeds they appear as conjugated forms. There is no clear role envisaged for these conjugated polyamines in plants, but scanty reports suggest their possible involvement in plant defence (Sridevi et al., 2009). Increased polyamine levels were observed during somatic embryogenesis of carrot cell cultures (Fienberg et al., 1984) and in developing tomato fruits (Heimer et al., 1979). L-Tyrosine decarboxylase (TYDC) belongs to the aromatic L-amino acid decarboxylase enzyme family and catalyses the conversion of tyrosine to tyramine in plants (Park et al., 2012).
Biochemical Effects in Animals
Published in Stephen P. Coburn, The Chemistry and Metabolism of 4′-Deoxypyridoxine, 2018
Hurwitz210 reported that 4′-deoxypyridoxine; 4,5-dihydroxymethyl-2-methyl-pyridoxine; and 3-amino-4,5-dihydroxymethyl-2-methylpyridine had no effect on tyrosine decarboxylase before phosphorylation but did inhibit after phosphorylation. The following compounds had no effect on the decarboxylase: 2-ethyl-3-amino-4-ethoxymethyl-5-aminomethylpyridine; 2-methyl-3-hydroxy-4-hydroxymethylpyridine; 3,4-dihydroxymethyl-2,6-dimethylpyridine; 3-amino-3-methyl-4,5,6-trihydroxymethylpyridine; 5-hydroxymethyl-2,4,6-trimethylpyridine; and 3-hydroxy-5,6-dihydroxy-methyl-2-methylpyridine. As was observed with the aminotransferases, neither 3- nor 4′-deoxypyridoxine produced significant inhibition if the enzyme was incubated with pyridoxal phosphate prior to the addition of the analog.
Phosphonic Acids And Phosphonates As Antimetabolites
Published in Richard L. Hilderbrand, The Role of Phosphonates in Living Systems, 2018
The species (92) has been found to have only minimal interaction with tyrosine decarboxylase,325 but to be very similar to the natural system in its interaction with aspartate aminotransferase.330 It has also been found that (93) and (94) are active for the reconstitution of rabbit muscle glycogen phosphorylase.326–327 Species (95) and (96) have been inactive in all systems tested to date.328
Circadian gating of light-induced arousal in Drosophila sleep
Published in Journal of Neurogenetics, 2023
Octopamine is one of the monoamine neurotransmitters in insects and is closely related to norepinephrine in mammals (Roeder, 2005). It is implicated in a broad range of insect physiology including aggression, motor behaviors, alcohol tolerance, metabolism, and arousal (Roeder, 2020; Selcho & Pauls, 2019). Octopamine biosynthesis requires tyrosine decarboxylase 2 (TDC2), which removes the carboxyl group from tyrosine, producing the octopamine precursor tyramine. Genetic deficiency in the octopamine biosynthesis pathway leads to long daytime sleep in Drosophila (Crocker & Sehgal, 2008). On the other hand, transgenic excitation of the TDC2-expressing octopaminergic neurons suppresses nighttime sleep, defining octopamine as a wake-promoting neurotransmitter (Crocker & Sehgal, 2008; Kayser et al., 2015). Intriguingly, most Drosophila octopaminergic neurons are also glutamatergic, and their co-transmission has been shown to play differential roles in aggression and courtship behaviors (Sherer et al., 2020). We thus asked if the dual neurotransmission would contribute to octopamine-relevant sleep regulation.
The gut-brain axis and Parkinson disease: clinical and pathogenetic relevance
Published in Annals of Medicine, 2021
Elisa Menozzi, Jane Macnaughtan, Anthony H. V. Schapira
Unfortunately, our understanding of the causative role of SIBO in PD remains unclear. In previous studies, several factors (such as lack of standardised protocols for breath tests for SIBO [111], or spontaneous changes in SIBO status during the disease course [107,112]), have limited interpretation. SIBO-positive patients may display increased intestinal permeability that facilitates bacterial translocation, creates a proinflammatory environment, and ultimately promotes microglial activation and neurodegeneration (e.g. abnormal accumulation of α-synuclein in enteric neurons) [111]. Alternatively, SIBO might affect levodopa bioavailability, either as a result of peripheral inflammation or partial metabolism of levodopa [63]. Recent studies reporting the effect of small intestine microbiome on peripheral levodopa conversion, supports this last hypothesis. The first step of bacterial levodopa metabolism, the decarboxylation of levodopa to dopamine, is in fact carried out by bacterial tyrosine decarboxylase (tyrDC), which is encoded on genomes of several species in the small intestine [113]. Among all the identified bacterial species, only Enterococcus faecalis was able to completely metabolise levodopa, and the abundance of Enterococcus faecalis and tyrDC correlated with levodopa and dopamine metabolism in human gut microbiota samples [114].
Trace amine associated receptor 1 (TAAR1) expression and modulation of inflammatory cytokine production in mouse bone marrow-derived macrophages: a novel mechanism for inflammation in ulcerative colitis
Published in Immunopharmacology and Immunotoxicology, 2019
Katlynn Bugda Gwilt, Neva Olliffe, Rachel A. Hoffing, Gregory M. Miller
Ulcerative colitis (UC) is a chronic relapsing inflammatory condition of the gastrointestinal tract (GIT) thought to be triggered by a dysregulated immune response in genetically susceptible patients to commensal microbiomic bacteria and certain dietary triggers [1]. Recent metabolomic studies in human patients with UC seeking to understand the metabolomic pathways of the microbiome involved in the propagation of UC found elevated tyramine (TYR) levels in patients with UC, compared to controls [2]. TYR occurs naturally in the body as a byproduct of tyrosine metabolism is found in certain food products and is produced by a variable subset of common microbiome organisms [3]. Bacteria common to the human microbiome possess tyrosine decarboxylase enzymatic systems that are capable of synthesizing TYR from tyrosine [4]. TYR has been studied for greater than a century, though it was not until 2001 that a receptor for TYR and other trace amines was identified [5,6]. Since its identification, trace amine-associated receptor 1 (TAAR1) has mainly been studied in the brain, while few studies have investigated its role in the immune cells [7–11]. There have been no investigations on TAAR1’s role in the lower GIT, where TYR traverses with stool at higher than normal levels in UC in human patients and mouse models of colitis [2,12]. The sources of TYR in the mouse GIT were found to be from both dietary sources and components of the host microbiome [13,14].