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Although the anhydrous compound is known, trimethylamine N-oxide is usually encountered as the dihydrate. Both the anhydrous and hydrated materials are white, water-soluble solids. TMAO is found in the tissues of marine crustaceans and marine fish, where it prevents water pressure from distorting proteins and thus killing
Trimethylamine N-oxide reductase has the EC number 1.7.2.3, and these components refer to the following enzyme classifications: EC 1 enzymes are oxidoreductase enzymes, where an oxidation reduction reaction occurs, and the substrate being oxidized is either an oxygen or hydrogen donor
Trimethylamine is a full agonist of human TAAR5, [13] [14] [15] a trace amine-associated receptor that is expressed in the olfactory epithelium and functions as an olfactory receptor for tertiary amines. [15] [16] One or more additional odorant receptors appear to be involved in trimethylamine olfaction in humans as well. [16]
Some marine fish, like sharks, have adopted a different, efficient mechanism to conserve water, i.e., osmoregulation. They retain urea in their blood in relatively higher concentration. Urea damages living tissues so, to cope with this problem, some fish retain trimethylamine oxide, which helps to counteract urea's destabilizing effects on ...
Their body fluid is isosmotic with seawater, but their high osmolarity is maintained by making the concentration of organic solutes unnaturally high. Sharks concentrate urea in their bodies, and since urea denatures proteins at high concentrations, they also accumulate trimethylamine N-oxide (TMAO) to counter the effect. Sharks adjust their ...
The trimethylaminuria disorder, also known as fish odor syndrome, causes abnormal FMO3-mediated metabolism or a deficiency of this enzyme in an individual. A person with this disorder has a low capacity to oxidize the trimethylamine (TMA) that comes from their diet to its odourless metabolite TMAO. [34]
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FMO3 is the primary enzyme in humans which catalyzes the N-oxidation of trimethylamine into trimethylamine N-oxide; [8] [10] FMO1 also does this, but to a much lesser extent than FMO3. [13] [14] Genetic deficiencies of the FMO3 enzyme cause primary trimethylaminuria, also known as "fish odor syndrome".