Relatively large amounts of nonvolatile higher amines are formed during proteolysis of fish muscle by bacteria. This follows closely the formation of trimethylamine. Fresh fish contain 0.2 mg. nitrogen per 100 g, muscle as trimethylamine and about 0.1 mg. nitrogen per 100 g. as dimethylamine. Trichloracetic acid and formaldehyde solutions completely extracted trimethylamine from fish and satisfactory recovery of added trimethylamine was obtained.

Trace amine-associated receptors (TAARs) are G Protein-Coupled Receptors that function as vertebrate olfactory receptors. Like odorant receptors, TAARs constitute an ever-evolving sensory subsystem, with individual TAARs recognizing particular chemicals and some evoking stereotyped behaviors. Several TAARs mediate aversion or attraction towards volatile amines that include the mouse odor trimethylamine, the predator odor 2-phenylethylamine, and the death-associated odor cadaverine. TAAR-expressing sensory neurons achieve monoallelic receptor expression, use canonical olfactory signaling molecules, and target a dedicated olfactory bulb region. In mouse, TAAR4 and TAAR5 are encoded by adjacent genes and localize to adjacent glomeruli, yet mediate opposing behaviors. Future studies are needed to understand how TAAR-expressing sensory neurons engage higher-order neural circuits to encode odor valence.

In addition to the canonical olfactory receptors, TAARs were currently suggested to be a second class of chemosensory receptors in the olfactory epithelium of vertebrates. In contrast to several deorphanized murine TAARs, agonists for the intact human TAAR genes 2, 5, 6, 8 and 9 that are potentially expressed in the human olfactory epithelium have not been determined so far. Moreover, the physiological relevance of TAARs still remains elusive. We present the first successful functional expression of a human TAAR and agonists of human TAAR5. We performed a ligand screening using recombinantly expressed human TAAR5 in HANA3A cells and Xenopus laevis oocytes. In order to measure receptor activity, we used a cAMP-dependent reporter gene assay and two-electrode voltage clamp technique. As a result, human TAAR5 can be activated in a concentration-dependent manner by trimethylamine and with less efficacy by dimethylethylamine. It could neither be activated by any other of the tested single amines with a related chemical structure (42 in total), nor by any of the tested odorant mixtures. The hypothesis that Single Nucleotide Polymorphisms (SNP) within the reading frame of an olfactory receptor gene can cause a specific anosmia, formed the basis for clarifying the question, if anosmia for trimethylamine is caused by a SNP in a TAAR coding sequence. All functional human TAAR gene reading frames of subjects with specific anosmia for trimethylamine were amplified and products analyzed regarding SNP distribution. We demonstrated that the observed specific anosmia for trimethylamine is not correlated with a SNP in the coding sequence of one of the putatively functional human TAAR genes.

The mammalian main olfactory pathway detects volatile chemicals using two families of G-protein-coupled receptors: a large repertoire of canonical odorant receptors and a much smaller set of trace amine-associated receptors (TAARs). The TAARs are evolutionarily conserved in vertebrates, including humans, suggesting an indispensible role in olfaction. However, little is known about the functional properties of TAARs when expressed in native olfactory sensory neurons. Here we describe experiments using gene targeting, electrophysiology, and optical imaging to study the response properties of TAAR-expressing sensory neurons and their associated glomeruli in mice. We show that olfactory sensory neurons that express a subset of the TAAR repertoire are preferentially responsive to amines. In addition, neurons expressing specific TAARs, TAAR3 or TAAR4, are highly sensitive and are also broadly tuned-responding to structurally diverse amines. Surprisingly, we find that TAAR4 is exquisitely sensitive, with apparent affinities for a preferred ligand, phenylethylamine, rivaling those seen with mammalian pheromone receptors. We provide evidence that this unprecedented sensitivity is mediated via receptor coupling to the canonical odorant transduction cascade. The data suggest that the TAARs are evolutionarily retained in the olfactory receptor repertoire to mediate high-sensitivity detection of a biologically relevant class of odorous stimuli.

Accumulating evidence indicates that microbiota plays a critical role in physiological processes in humans. However, it might also contribute to body malodor by producing numerous odorous molecules such as ammonia, volatile sulfur compounds or trimethylamine. Although malodor is commonly overlooked by physicians, it constitutes a major problem for many otherwise healthy people. Thus, this review aims to investigate most common causes of malodor and describe potential therapeutic options. We searched PUBMED and Google Scholar databases to identify the clinical and pre-clinical studies on bad body smell, malodor, halitosis and microbiota. Unpleasant smell might originate from the mouth, skin, urine or reproductive fluids and is usually caused by odorants that are produced by resident bacterial flora. The accumulation of odorous compounds might result from diet, specific composition of microbiota, as well as compromised function of the liver, intestines and kidneys. Evidence-based guidelines for management of body malodor are lacking and no universal treatment exists. However, the alleviation of the symptoms may be achieved by controlling the diet and physical elimination of bacteria and/or accumulated odorants.

Sense of smell in humans has the capacity to detect certain volatiles from bacterial infections. Our olfactory senses were used in ancient medicine to diagnose diseases in patients. As humans are considered holobionts, each person's unique odor consists of volatile organic compounds (VOCs, volatilome) produced not only by the humans themselves but also by their beneficial and pathogenic micro-habitants. In the past decade it has been well documented that microorganisms (fungi and bacteria) are able to emit a broad range of olfactory active VOCs [summarized in the mVOC database (http://bioinformatics.charite.de/mvoc/)]. During microbial infection, the equilibrium between the human and its microbiome is altered, followed by a change in the volatilome. For several decades, physicians have been trying to utilize these changes in smell composition to develop fast and efficient diagnostic tools, particularly because volatiles detection is non-invasive and non-destructive, which would be a breakthrough in many therapies. Within this review, we discuss bacterial infections including gastrointestinal, respiratory or lung, and blood infections, focusing on the pathogens and their known corresponding volatile biomarkers. Furthermore, we cover the potential role of the human microbiota and their volatilome in certain diseases such as neurodegenerative diseases. We also report on discrete mVOCs that affect humans.

Total volatile basic nitrogen (TVBN), biogenic amine, total viable count (TVC), volatile compounds, and sensory evaluation were conducted to assess the quality of Chinese Mitten Crabs (<i>Eriocheir sinensis</i>) at living, zero, 2, 5, 10, 15, and 24 hr postmortem. The sensory evaluation found a noticeable odor of spoilage becoming evident 10 hr postmortem. The TVBN value increased and then decreased as time increased, reaching 23.67 mg N/100 g at 24 hr postmortem. Although biogenic amines were detected at 5 hr postmortem, by 24 hr postmortem these had not reached dangerous levels of toxicity. The initial TVC (6.06 Log CFU/g) of the living crab samples was relatively high and climbed further postmortem, reaching 10.00 Log CFU/g 24 hr postmortem. Trimethylamine was detected in the living sample in belly meat and 2 hr postmortem in crab roe and reached 8.33 µg/g in the roe 24 hr postmortem. Indole was detected at 0 hr (belly meat) and 10 hr (crab roe) postmortem, but did not change significantly during the observation period. Sulfur-containing compounds were detected 5 hr after death and gradually increased over the observation period. Most indicators showed major changes at 5 hr and 10 hr postmortem. By 10 hr postmortem, the crab had entered the putrefaction stage and was thus no longer safe for consumption.

trimethylaminuria develop a characteristic fish odor—the smell of trimethylamine—in their sweat, urine, and breath after the consumption of choline-rich Trimethylamine (TMA) is an organic compound with the formula N(CH3)3. It is a trimethylated derivative of ammonia. TMA is widely used in industry. At higher concentrations it has an ammonia-like odor, and can cause necrosis of mucous membranes on contact. At lower concentrations, it has a "fishy" odor, the odor associated with rotting fish. Trimethylamine (TMA) is an organic compound with the formula N(CH3)3. It is a trimethylated derivative of ammonia. TMA is widely used in industry. At higher concentrations it has an ammonia-like odor, and can cause necrosis of mucous membranes on contact. At lower concentrations, it has a "fishy" odor, the odor associated with rotting fish. Trimethylaminuria is an autosomal recessive genetic disorder involving a defect in the function or expression of flavin-containing monooxygenase 3 (FMO3) which results in poor trimethylamine metabolism. Individuals with trimethylaminuria develop a characteristic fish odor—the smell of trimethylamine—in their sweat, urine, and breath after the consumption of choline-rich foods. A condition similar to trimethylaminuria has also been observed in a certain breed of Rhode Island Red chicken that produces eggs with a fishy smell, especially after eating food containing a high proportion of rapeseed.

Research progress of fishy odor in aquatic products: From substance identification, formation mechanism, to elimination pathway - PubMed Save Email Send to Display options Full text links Cite Display options ## Abstract Fishy odor in aquatic products has a significant impact on the purchasing decisions of consumers. The production of aquatic products is a complex process involving culture, processing, transportation, and storage, which contribute to decreases in flavor and quality. This review systematically summarizes the fishy odor composition, identification methods, generation mechanism, and elimination methods of fishy odor compounds from their origin and formation to their elimination. Fishy odor compounds include aldehydes (hexanal, heptanal, and nonanal), alcohols (1-octen-3-ol), sulfur-containing compounds (dimethyl sulfide), and amines (trimethylamine). The mechanism of action of various factors affecting fishy odor is revealed, including environmental factors, enzymatic reactions, lipid oxidation, protein degradation, and microbial metabolism. Furthermore, the control and removal of fishy odor are briefly summarized and discussed, including masking, elimination,

s ) or strong-smelling pee. Sometimes, people only notice TMAU symptoms when the person who has the condition sweats or is experiencing stress. But some people with trimethylaminuria carry such a strong scent that others notice the scent just from being in the same room, standing across a counter or sitting in the same section of a bus or train. Advertisement What causes TMAU? Trimethylaminuria happens when something affects the FMO3 enzyme so it doesn’t work like it should. FMO3 stands for flavin-containing monooxygenase 3. This enzyme manages the impact that trimethylamine has on your body. Trimethylamine is a smelly chemical your body produces when you eat certain foods like fish, beans and eggs. Normally, there’s a check-and-balance relationship between trimethylamine and FMO3: when your body produces trimethylamine, FMO3 enzymes break it down. That way, the chemical doesn’t smell bad when it moves from your digestive system into your bloodstream. When that doesn’t happen, trimethylamine builds up in your body, eventually seeping into your system so that your breath, sweat, saliva and pee smell like rotten fish. People with primary trimethylaminuria develop the condition because they inherit abnormal FMO3 genes from both of their biological parents. In secondary TMAU, something keeps your FMO3 enzyme from breaking down trimethylamine. This can happen if: You have an illness, like liver failure or viral hepatitis , that keeps the enzyme from breaking down the trimethylamine. There’s an imbalance in your gut microbiome so there’s more trimethylamine in your system than the FMO3 enzymes can change into the non-smelly version of the chemical. You take choline or carnitine supplements. These nutrients play a role in producing trimethylamine. What are complications of this condition? Trimethylaminuria can damage your quality of life. Research shows people with the condition often avoid relationships, jobs and activities where others may notice the unpleasant smell tha