trimethylamine


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Related to trimethylamine: Trimethylamine oxide, Trimethylamine N-oxide

tri·meth·yl·am·ine

(trī-meth'il-am'ēn),
A degradation product, often by putrefaction, of nitrogenous plant and animal substances (for example, beet sugar residue or herring brine); in the body, it probably results from decomposition of choline.

tri·meth·yl·am·ine

(trī-meth'il-am'ēn)
A degradation product, often by putrefaction, of nitrogenous plant and animal substances such as beet sugar residue or herring brine; in the body, it probably results from decomposition of choline.
References in periodicals archive ?
Deprotonation is achieved by the addition of trimethylamine to the reaction mixture.
Comparative characteristics of KOR-2 strain isolated from the rumen of Holstein steers (1) Characteristics KOR-2 MS2T Cell morphology Coccoid Coccoid Cell width ([micro]m) 0.2-0.5 1.0-2.0 Temperature for growth ([degrees]C) Range 25-45 30-49 Optimum 38 37 pH for growth Range 4.0-9.0 5.5-8.0 Optimum 6.8-7.0 6.7 NaCl for growth range (%) Range 0.5-3.0 0-4.0 Optimum 1.0 1.0 DNA G+C content (mol%) (2) 55.5 (Tm) 59 (Bd) Substrate utilization [H.sub.2]/C[O.sub.2] + + Formate + + Acetate - - Methanol - - Trimethylamine - - 2-propanol - - Isobutanol - - Tolerance for antibiotics Ampicillin + ND Penicillin G + ND Spectromycin + ND Kanamycin + ND Tetracycline + ND Chloramphenicol - ND -, negative; +, positive; ND, no data available.
We found lower levels of metabolites from the methylamine pathway; trimethylamine is derived from dietary choline fermentation by commensal bacteria and metabolized into trimethylamine oxide in the liver (Craciun and Balskus 2012).
The disparity of FA for all types of fish samples analysed could be explained on the bases that different species have a different amount of trimethylamine oxide (TMAO) even if intentional addition of FA to prolong the shelf life and maximised profit was not considered.
PC, like carnitine from red meat, is converted by intestinal bacteria into trimethylamine. Trimethylamine is oxidized in the liver to trimethylamine N-oxide (TMAO), and TMAO increases in a dose-dependent manner with egg consumption [174].
In this review, we aimed to discuss the compositional and functional changes in the gut microbiota in relation to CVD, determine the effects of the gut microbiota on CVD from the view of trimethylamine N-oxide (TMAO) and immune cells, and evaluate how gut interventions can lead to novel therapeutic targets for CVD.
The expression of abundant proteins mttBC/mtbA for trimethylamine, mtbBC/ mtbA for dimethylamine, mtmBC/mtbA for monomethylamine, and mtaABC for methanol revealed the activities of M.
also reported a dinuclear cobalt(II) complex of calix[8] arenes compound, prepared by solvothermal reaction of cobalt(II) acetate with p-t-butylcalix[8]arene and trimethylamine; the compound was formed by hydrogen bond bridging [33].
Intestinal metabolites such as hydrogen sulfide (H2S), SCFA, indole, or trimethylamine may exert effects on circulatory system homeostasis and on nerve and humoral control.
Trimethylamine N-oxide (TMAO) is a plasma metabolite from nutrient precursors (choline, phosphatidylcholine, and L-carnitine), which is produced by gut microbiota.
Trimethylamine oxides are also found within the red muscle that can be enzymatically or nonenzymatically degraded, resulting in products such as dimethylamine (DA) and formaldehyde (FA) [39, 40].
For example, a gut-derived metabolite, trimethylamine N-oxide, directly induces platelet hyperactivity and increases thrombosis potential.