The nomenclature of pyrimidines is straightforward. However, like other heterocyclics, tautomeric hydroxyl groups yield complications since they exist primarily in the cyclic amide form. 65-86-1, formula is C5H4N2O4, Name is 2,6-Dioxo-1,2,3,6-tetrahydropyrimidine-4-carboxylic acid. For example, 2-hydroxypyrimidine is more properly named 2-pyrimidone. A partial list of trivial names of various pyrimidines exists. SDS of cas: 65-86-1.
Solmonson, Ashley;Faubert, Brandon;Gu, Wen;Rao, Aparna;Cowdin, Mitzy A.;Menendez-Montes, Ivan;Kelekar, Sherwin;Rogers, Thomas J.;Pan, Chunxiao;Guevara, Gerardo;Tarangelo, Amy;Zacharias, Lauren G.;Martin-Sandoval, Misty S.;Do, Duyen;Pachnis, Panayotis;Dumesnil, Dennis;Mathews, Thomas P.;Tasdogan, Alpaslan;Pham, An;Cai, Ling;Zhao, Zhiyu;Ni, Min;Cleaver, Ondine;Sadek, Hesham A.;Morrison, Sean J.;DeBerardinis, Ralph J. research published 《 Compartmentalized metabolism supports midgestation mammalian development》, the research content is summarized as follows. Mammalian embryogenesis requires rapid growth and proper metabolic regulation. Midgestation features increasing oxygen and nutrient availability concomitant with fetal organ development. Understanding how metabolism supports development requires approaches to observe metabolism directly in model organisms in utero. Here we used isotope tracing and metabolomics to identify evolving metabolic programs in the placenta and embryo during midgestation in mice. These tissues differ metabolically throughout midgestation, but we pinpointed gestational days (GD) 10.5-11.5 as a transition period for both placenta and embryo. Isotope tracing revealed differences in carbohydrate metabolism between the tissues and rapid glucose-dependent purine synthesis, especially in the embryo. Glucoses contribution to the tricarboxylic acid (TCA) cycle rises throughout midgestation in the embryo but not in the placenta. By GD12.5, compartmentalized metabolic programs are apparent within the embryo, including different nutrient contributions to the TCA cycle in different organs. To contextualize developmental anomalies associated with Mendelian metabolic defects, we analyzed mice deficient in LIPT1, the enzyme that activates 2-ketoacid dehydrogenases related to the TCA cycle. LIPT1 deficiency suppresses TCA cycle metabolism during the GD10.5-GD11.5 transition, perturbs brain, heart and erythrocyte development and leads to embryonic demise by GD11.5. These data document individualized metabolic programs in developing organs in utero.
65-86-1, Orotic acid anhydrous is a hydrogen bonding interaction that can be found in biological systems. It plays a role in the physiological effects of orotic acid, which is a metabolite of uridine and an intermediate in the synthesis of pyrimidine nucleotides. Orotic acid has antimicrobial properties and has been shown to inhibit enzyme activities involved in energy metabolism, such as polymerase chain reaction (PCR) and adenosine triphosphate (ATP) synthase. Orotic acid also inhibits the growth of bacteria, fungi, and parasites. Orotic acid anhydrous is used for treating myocardial infarcts or brain functions. The untreated group was given no treatment at all.
Orotic acid, also known as orotate or orotsaeure, belongs to the class of organic compounds known as pyrimidinecarboxylic acids. These are pyrimidines with a structure containing a carboxyl group attached to the pyrimidine ring. Orotic acid exists as a solid, slightly soluble (in water), and a moderately acidic compound (based on its pKa). Orotic acid has been found in human liver and pancreas tissues, and has also been primarily detected in saliva, feces, urine, and blood. Within the cell, orotic acid is primarily located in the cytoplasm and mitochondria. Orotic acid exists in all eukaryotes, ranging from yeast to humans. Orotic acid participates in a number of enzymatic reactions. In particular, Orotic acid can be biosynthesized from L-dihydroorotic acid and quinone; which is mediated by the enzyme dihydroorotate dehydrogenase (quinone), mitochondrial. In addition, Orotic acid and phosphoribosyl pyrophosphate can be converted into orotidylic acid through its interaction with the enzyme uridine monophosphate synthetase isoform a. In humans, orotic acid is involved in the pyrimidine metabolism pathway. Orotic acid is also involved in several metabolic disorders, some of which include the mngie (mitochondrial neurogastrointestinal encephalopathy) pathway, dihydropyrimidinase deficiency, UMP synthase deficiency (orotic aciduria), and Beta ureidopropionase deficiency. Outside of the human body, orotic acid can be found in a number of food items such as green vegetables, alaska blueberry, chickpea, and colorado pinyon. This makes orotic acid a potential biomarker for the consumption of these food products. Orotic acid is a potentially toxic compound. Orotic acid has been found to be associated with several diseases known as phosphoenolpyruvate carboxykinase deficiency 1, cytosolic and hyperornithinemia-hyperammonemia-homocitrullinuria; orotic acid has also been linked to several inborn metabolic disorders including n-acetylglutamate synthetase deficiency, lysinuric protein intolerance, and ornithine transcarbamylase deficiency.
Orotic acid appears as white crystals or crystalline powder.
Orotic acid is a pyrimidinemonocarboxylic acid that is uracil bearing a carboxy substituent at position C-6. It has a role as a metabolite, an Escherichia coli metabolite and a mouse metabolite. It derives from a uracil. It is a conjugate acid of an orotate., SDS of cas: 65-86-1
Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia