Induction of Controlled Differentiation of Callus in Mosses
R. N. Chopra, Satish C. Bhatla in Bryophyte Development: Physiology and Biochemistry, 2019
Moss callus cells derived from the hybrid sporogonium were also used to study the developmental physiology as influenced by light and its various spectral components.47 In the heterogeneous nature of the morphogenetic effects of light it was shown that under red light the RNA and protein contents increased, whereas under blue light the highest chlorophyll content was observed in relation to plastid development. Blue light enhanced the amino acid metabolism, whereas red light was found to affect carbon metabolism. This had been demonstrated by the existence of heterotrophy with regard to nitrogen and sugar. As an accumulation product of nitrogen metabolism allantoin was formed, and this is a typical expression of moss callus heterotrophy. This metabolic product could be distinctly connected with purine metabolism; this was proved by feeding 14C-adenine to the culture. In darkness tryptophan content is significantly higher, whereas in white light α-aminobutyric acid and proline attain very high concentrations. In red light tyrosine was observed to be present in higher amounts in these hybrid callus cells.47 In the protonemal callus of Physcomitrium pyriforme it could be demonstrated that 14C-proline is rapidly converted to hydroxyproline. This was found to be noncovalently linked to the cell wall and could be extracted with chaotropic salts. This showed the presence of a glycoprotein rich in hydroxyproline in the callus cell wall.48
Kidneys and ureters
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
Uric acid stones account for approximately 5-10% of urinary tract stones. Patients with uric acid stones either excrete excessive amounts of uric acid or have excessively acid urine and uric acid remains undissociated and insoluble at pH <5.5. Uric acid is an end-product of purine metabolism. Dietary purine and protein excesses may increase urinary uric acid excretion. Extensive cellular turnover in myeloproliferative diseases or in those receiving chemotherapy may result in increased uric acid production. Uric acid stones can also occur in patients with normal serum uric acid levels (idiopathic uric acid lithiasis). Low urine volume may contribute to uric acid stone disease, such as in patients with inflammatory bowel disease and ileostomies. Uric acid stones are hard, smooth, often multiple and are multifaceted. Pure uric acid stones are radiolucent but most uric acid stones contain some calcium and are consequently faintly radio-opaque.
Thymus Influence on Differentiation and Functional Maturation of T Lymphocytes
Marek P. Dabrowski, Barbara K. Dabrowska-Bernstein in Immunoregulatory Role of Thymus, 2019
Three purine metabolism enzymes, adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), and 5′ nucleotidase (5′NT), as well as terminal deoxynucleotidyl transferase (TdT), are thought to be important for normal lymphocyte development.63. Impairment of T cell development and/or T and B cell functions have been reported in congenital ADA and PNP deficiencies or to be concomitant to 5′ NT deficiency. No congenital deficiency of TdT has been described in humans; nevertheless, this enzyme appears to be important for T cell development since it is present only at the early stages of maturation in bone marrow-derived T cell precursors and cortical thymocytes. Ma et al.63 have collected a quantity of impressive arguments indicating that a particular constellation of these enzymes in cortical thymocytes may account for the cell biochemical suicide, thus explaining the high cellular death rate in the thymus.
Purine metabolites can indicate diabetes progression
Published in Archives of Physiology and Biochemistry, 2022
Yogaraje Gowda C. Varadaiah, Senthilkumar Sivanesan, Shivananda B. Nayak, Kashinath R. Thirumalarao
Purines are fundamental parts of nucleotides and nucleic acids, playing numerous important roles in human physiology, disturbing tissue function, cell integrity and oxidation. Purine metabolism comprises of synthesis and degradation of purine nucleotides and regulates the level of the adenylate and guanylate pool (Dudzinska et al. 2010). In this way, it is responsible for the complete concentrations of intracellular ATP and GTP. In purine catabolism, their monophosphate forms are transformed to inosine and guanosine; purine nucleoside phosphorylase changes them to hypoxanthine and guanine, respectively (Figure 1). Xanthine oxidase (XO) and guanine deaminase are the enzymes that convert them to xanthine which is oxidized by XO to uric acid (Maiuolo et al. 2016). Serum uric acid, an end product of purine metabolism, has been shown to be associated with an increased risk of hypertension, cardiovascular disease, and chronic kidney disease. Hyperuricemia raises the risk of peripheral arterial disease, insulin resistance, and components of the metabolic syndrome (Ekpenyong and Akpan 2014). In diabetes, hyperuricemia has been associated with both micro and macrovascular complications. It is well known that purine metabolic pathway may be strongly linked with the development of diabetic microvascular complications (Xia et al. 2014).
Recent approaches to gout drug discovery: an update
Published in Expert Opinion on Drug Discovery, 2020
Naoyuki Otani, Motoshi Ouchi, Hideo Kudo, Shuichi Tsuruoka, Ichiro Hisatome, Naohiko Anzai
Purine bases are synthesized as nucleotides linked to ribose-5-phosphate (R5P). Purine nucleotides are the substrate for the synthesis of adenosine triphosphate (ATP), which is the energy source of cells, a component of the DNA and RNA, an enzyme cofactor in regulatory and metabolic pathways, and the substrate for regenerating cyclic adenosine monophosphate (cAMP), guanosine triphosphate (GTP), and cyclic guanosine monophosphate (cGMP), which all fulfil critical roles in intracellular signal transduction. Purine metabolism is governed by complex metabolic regulatory mechanisms, including the de novo purine nucleotide synthesis pathway, which generates purine skeletons from phosphoribosyl pyrophosphate (PRPP), and the salvage pathway for purine nucleotide synthesis from free purine bases.
Inosine induces acute hyperuricaemia in rhesus monkey (Macaca mulatta) as a potential disease animal model
Published in Pharmaceutical Biology, 2021
Dong-hong Tang, Chen-yun Wang, Xi Huang, Hong-kun Yi, Zhe-li Li, Kai-li Ma, You-song Ye, Jian-wen Zhang
Uric acid production and metabolism are complex processes involving various factors that regulate uric acid production in the liver and reabsorption or excretion from the kidneys and gut (Mori and Percudani 2016; Yun et al. 2017). The balance of these processes maintains uric acid homeostasis. Several enzymes are involved in the conversion of the purine nucleotides adenine and guanine to uric acid, including purine nucleoside phosphorylase (PNP) and xanthine oxidase (XO), which catalyse the formation of xanthine, and subsequently, uric acid, respectively (Magness et al. 2005; Yan et al. 2011). Furthermore, these enzymes catalyse the conversion of adenosine and inosine, which are precursors of purine metabolism. Similarly, the conversion of guanosine is catalysed by these enzymes to guanine, xanthine and, finally, to uric acid. Therefore, an abnormal activity of these enzymes can lead to increased uric acid production, leading to HUA (Ishikawa et al. 2013).
Related Knowledge Centers
- Adenine
- Glycine
- Metabolic Pathway
- Nucleotide
- Purine
- Nitrogen
- Guanine
- Ribose 5-Phosphate
- Inosinic Acid
- Carbon