PathWhiz

PathWhiz ID	Pathway	Meta Data
PW124605 View Pathway	metabolic Metabolism and Physiological Effects of Phenol Homo sapiens Phenol is a phenolic compound that is formed through gut microbial metabolism from dietary tyrosine. After being transported into gut microbes, tyrosine undergoes a reaction with the enzyme tyrosine phenol-lyase to form phenol. Phenol that is produced from the gut microbes then enters systemic circulation. Phenol can get further metabolized in a liver hepatocyte to Phenyl sulphate and Phenyl glucuronide. However phenol itself is shown to be a major uremic toxin through high levels of retention. Phenol is shown to cause cardiovascular disease and enhance the production of reactive oxygen species and cause oxidative stress. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Rahil Doshi Created On: March 24, 2021 at 01:11 Last Updated: March 24, 2021 at 01:11
PW128449 View Pathway	metabolic Metabolism and Physiological Effects of Phenol sulphate Homo sapiens Phenol sulphate, also known as phenylsulfate or aryl sulphate, belongs to the class of organic compounds known as phenylsulfates. Phenylsulfates are compounds containing a sulfate group conjugated to a phenyl group. In normal humans, phenol sulphate is primarily a gut-derived metabolite that arises from the activity of the bacterial enzyme tyrosine phenol-lyase, which is responsible for the synthesis of phenol from dietary tyrosine. Phenol sulphate can also arise from the consumption of phenol or from phenol poisoning. Phenol sulphate is produced from the conjugation of phenol with sulphate in the liver. In particular, phenol sulphate can be biosynthesized from phenol and phosphoadenosine phosphosulfate through the action of the enzyme sulfotransferase 1A1 in the liver. Phenol sulphate can be found in most mammals (mice, rats, sheep, dogs, humans) and likely most animals. Phenol sulphate is a uremic toxin. It is a protein-bound uremic solute that induces reactive oxygen species (ROS) production and decreases glutathione levels, rendering cells vulnerable to oxidative stress. In experimental models of diabetes, phenol sulphate administration has been shown to induce albuminuria and podocyte damage. In a diabetic patient cohort, phenol sulphate levels were found to significantly correlate with basal and predicted 2-year progression of albuminuria in patients with microalbuminuria. Tyrosine is converted to phenol by a bacterial enzyme called tyrosine phenol-lyase before it is converted to phenol sulphate in the liver by sulfotransferase 1A1. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Hayley Created On: August 29, 2023 at 10:45 Last Updated: August 29, 2023 at 10:45
PW124577 View Pathway	metabolic Metabolism and Physiological Effects of Phenyl glucuronide Homo sapiens Phenyl glucuronide is a phenolic compound that is formed through gut microbial metabolism from dietary tyrosine and a glucuronidation reaction in liver hepatic cells. After being transported into gut microbes, tyrosine undergoes a reaction with the enzyme tyrosine phenol-lyase to form phenol. Phenol that is produced from the gut microbes then enters systemic circulation. Ultimately phenol undergoes a reaction in a liver hepatocyte through a glucuronosyltransferase enzyme to form Phenyl glucuronide. When this compound returns back into systemic circulation it is shown to be a major uremic toxin through high levels of retention. Phenyl glucuronide is shown to BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Rahil Doshi Created On: March 10, 2021 at 17:32 Last Updated: March 10, 2021 at 17:32
PW124563 View Pathway	metabolic Metabolism and Physiological Effects of Phenyl sulfate Homo sapiens Phenyl sulphate is a phenolic compound that is formed through gut microbial metabolism from dietary tyrosine and a sulfation reaction in liver hepatic cells. After being transported into gut microbes, tyrosine undergoes a reaction with the enzyme tyrosine phenol-lyase to form phenol. Phenol that is produced from the gut microbes then enters systemic circulation. Ultimately phenol undergoes a sulfation reaction in a liver hepatocyte through a sulfotransferase enzyme to form Phenyl sulphate. When Phenyl sulphate returns back into systemic circulation it is shown to be a major uremic toxin through high levels of retention. Phenyl sulphate is shown to cause albuminuria and diabetic kidney disease. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Rahil Doshi Created On: March 02, 2021 at 01:29 Last Updated: March 02, 2021 at 01:29
PW124606 View Pathway	metabolic Metabolism and Physiological Effects of Phenylacetic Acid Homo sapiens Phenylacetic acid is carboxylic acid ester that has also been found to be a uremic toxin that is synthesized from L-phenylalanine. L-Phenylalanine is consumed through high protein foods such as eggs, chicken, liver, beef, milk, and soybeans. In the intestine L-phenylalanine is converted into 2-phenylethylamine by the enzyme Aromatic-L-amino-acid decarboxylase. 2-Phenylethylamine then is transported into the periplasm of intestinal bacteria such as E. Coli strain K12 through an unknown transporter. In the periplasm of the E. coli, 2-phenylethylamine is catalyzed by the enzyme primary amine oxidase to synthesize phenylacetaldehyde. Phenylacetaldehyde is transported into the cytosol of the E. coli bacteria where it is catalyzed by the enzyme phenylacetaldehyde dehydrogenase to synthesize phenylacetic acid. Phenylacetic acid is transported out of the bacteria, back into the intestine by an unknown transporter. Phenylacetic acid is then transported into the blood where it has various effects on the human body. It reduces nitric oxide production and reduces protection against inflammation in vessel walls. It also leads to the production of reactive oxygen species. It also contribute to inflammation by priming polymorphonuclear leucocytes. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Rahil Doshi Created On: March 24, 2021 at 01:47 Last Updated: March 24, 2021 at 01:47
PW124558 View Pathway	metabolic Metabolism and Physiological Effects of Phenylacetylglutamine Homo sapiens Phenylacetylglutamine is a product formed by the conjugation of phenylacetate and glutamine. It is a common metabolite that occurs naturally in human urine. The highly-nitrogenous compound is most commonly encountered in human subjects with urea cycle disorders,. These conditions, such as uremia or hyperammonemia, tend to cause high levels of nitrogen in the form of ammonia in the blood. Uremic conditions are a result of defects in enzymes that convert ammonia to urea, the primary nitrogenous waste metabolite in the urea cycle. Phenylacetylglutamine is a product formed from the conjugation of phenylacetate and glutamine. Technically, it is the amino acid acetylation product of phenylacetate (or phenylbutyrate after beta-oxidation). Phenylacetylglutamine is a normal constituent of human urine, but other mammals such as the dog, cat, rat, monkey, sheep, and horse do not excrete this compound. Phenylacetyl-CoA and L-glutamine react to form phenylacetylglutamine and coenzyme A. The enzyme (glutamine N-acetyl transferase) that catalyzes this reaction has been purified from human liver mitochondria and shown to be a polypeptide species distinct from glycine-N-acyltransferase. Phenylacetylglutamine is a major nitrogenous metabolite that accumulates in uremia. It has been shown that over 50% of urine phenylacetylglutamine may be derived from kidney conjugation of free plasma phenylacetic acid and/or from the kidney's preferential filtration of conjugated phenylacetic acid. Phenylacetylglutamine is a microbial metabolite found in Christensenellaceae, Lachnospiraceae and Ruminococcaceae. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Rahil Doshi Created On: February 27, 2021 at 20:19 Last Updated: February 27, 2021 at 20:19
PW128465 View Pathway	metabolic Metabolism and Physiological Effects of Phenylacetylglycine Homo sapiens Phenylacetylglycine is an acyl glycine. Acyl glycines are normally minor metabolites of fatty acids. However, the excretion of certain acyl glycines is increased in several inborn errors of metabolism. In certain cases the measurement of these metabolites in body fluids can be used to diagnose disorders associated with mitochondrial fatty acid beta-oxidation. Acyl glycines are produced through the action of glycine N-acyltransferase (EC 2.3.1.13) which is an enzyme that catalyzes the chemical reaction:. acyl-CoA + glycine < -- > CoA + N-acylglycine. Phenylacetylglycine or PAG is a glycine conjugate of phenylacetic acid. Phenylacetic acid may arise from exposure to styrene (plastic) or through the consumption of fruits and vegetables. Phenylacetic acid is used in some perfumes, possessing a honey-like odour in low concentrations, and is also used in penicillin G production. PAG is a putative biomarker of phospholipidosis. Urinary PAG is elevated in animals exhibiting abnormal phospholipid accumulation in many tissues and may thus be useful as a surrogate biomarker for phospholipidosis. The presence of phenylacetylglycine in urine has been confirmed for dogs, rats and mice. However, the presence of this compound in human urine is controversial. GC-MS studies have not found this compound, while NMR studies claimed to have identified it. Glycine N-Phenylacetyltransferase is a mitochondrial acyltransferase which transfers the acyl group to the N-terminus of glycine (glycine + phenylacetyl-CoA = CoA + H+ + phenylacetylglycine). Can conjugate a multitude of substrates to form a variety of N-acylglycines. Phenylacetyl-CoA comes from the metabolism of phenylalanine. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Hayley Created On: August 30, 2023 at 08:50 Last Updated: August 30, 2023 at 08:50
PW128471 View Pathway	metabolic Metabolism and Physiological Effects of Phenylacetylglycine test Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Eponine Oler Created On: August 30, 2023 at 10:30 Last Updated: August 30, 2023 at 10:30
PW124626 View Pathway	metabolic Metabolism and Physiological Effects of Putrescine Homo sapiens Putrescine is an aliphatic amine that is formed through gut microbial metabolism from the amino acid arginine which is acquired from foods that are high in protein. After being transported into gut microbes, arginine undergoes 2 reactions with the enzymes Arginase and Ornithine Decarboxylase to form putrescine. Like other polyamines such as spermidine and spermine, putrescine can also be obtained directly from diet as well. While putrescine is important for interactions and processes involving, DNA, RNA and proteins, at high levels it is also a protein bound uremic toxin found in the body that can inhibit erythropoietin production which can eventually lead to anemia. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Rahil Doshi Created On: April 03, 2021 at 16:07 Last Updated: April 03, 2021 at 16:07
PW124599 View Pathway	metabolic Metabolism and Physiological Effects of Quinolinic Acid Homo sapiens Quinolinic acid is an indole uremic toxin compound that is formed through metabolism from dietary tryptophan in liver hepatic cells. After being transported into a hepatocyte from portal circulation the amino acid tryptophan undergoes a multi-step reaction with the enzymes tryptophan-2,3-dioxygenase, kynurenine 3-monooxygenase, kynureninase, and 3-hydroxyanthranilate 3,4-dioxygenase to form quinolinic acid. When this compound enters into systemic circulation it is shown to be a major uremic toxin when high levels of it are retained in the blood and not excreted in urine. Quinolinic acid is shown to have major neurotoxic effects on the brain by acting as an NMDA receptor agonist, causing excessive glutamate release and lipid peroxidation. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Rahil Doshi Created On: March 23, 2021 at 01:50 Last Updated: March 23, 2021 at 01:50