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Purine Metabolism: Uric Acid Synthesis, Degradation, and Associated Disorders, Study Guides, Projects, Research of Biochemistry

B.Tech Biotechnology 4th Semester Biochemistry Metabolism.

Typology: Study Guides, Projects, Research

2020/2021

Available from 07/22/2021

Devashish_Kalambe
Devashish_Kalambe ๐Ÿ‡ฎ๐Ÿ‡ณ

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๏‚ž The end product of purine metabolism in humans is uric acid. ๏‚ž The nucleotide monophosphates (AMP, IMP & GMP) are converted to their respective nucleoside forms (adenosine, inosine & guanosine) by the action of nucleotidase. ๏‚ž The amino group, either from AMP or adenosine, can be removed to produce IMP or ionosine.

๏‚ž Xanthine oxidase converts hypoxanthine to xanthine & xanthine to uric acid. ๏‚ž This enzyme contains FAD, molybdenum & iron. ๏‚ž It is exclusively found in liver & small intestine. ๏‚ž Xanthine oxidase liberates H2O2 which is harmful to the tissues. ๏‚ž Catalase cleaves H2O2 to H2O & O2.

๏‚ž It is final excretory product of purine metabolism in humans. ๏‚ž Uric acid can serve as an important antioxidant by getting itself converted (non-enzymatically) to allantoin. ๏‚ž It is believed that the antioxidant role of ascorbic acid in primates is replaced by uric acid.

๏‚ž Most animals (other than primates) oxidize uric acid by the enzyme uricase to allantoin, where the purine ring is cleaved. ๏‚ž Allantoin is then converted to allantoic acid & excreted in some fishes. ๏‚ž Further degradation of allantoic acid may occur to produce urea (in amphibians, most fishes & some molluscs) & to ammonia (in marine invertebrates).

Uric Acid Allantoin Allantoic acid Urea Ammonia Uricase Allantoinase Allantoicase Urease Glyoxylate

๏‚ž Hyperuricemia refers to an elevation in the serum uric acid concentration. ๏‚ž This is sometimes associated with increased uric acid excretion (uricosuria).

๏‚ž It is a metabolic disease associated with overproduction of uric acid. ๏‚ž At the physiological pH, uric acid is found in a more soluble form as sodium urate. ๏‚ž In severe hyperuricemia, crystals of sodium urate get deposited in the soft tissues, particularly in the joints. ๏‚ž Such deposits are commonly known as tophi.

๏‚ž PRPP synthetase: ๏‚ž In normal circumstances, PRPP synthetase is under feedback control by purine nucleotides (ADP & GDP). ๏‚ž A variant forms of PRPP synthetase-which are not subjected to feedback regulation-leads to the increased production of purines.

๏‚ž PRPP glutamylamidotransferase: ๏‚ž The lack of feedback control of this enzyme by purine nucleotides also leads to their elevated synthesis. ๏‚ž Deficiency of enzymes of salvage pathway: ๏‚ž HGPRT enzyme of purine salvage pathway & its defect causes Lesch-Nyhan syndrome. ๏‚ž It is associated with increased synthesis of purine nucleotides.

๏‚ž Glucose- 6 - phosphatase deficiency: ๏‚ž This condition is known as von Gierke's disease (glycogen storage disease, type I) ๏‚ž When this enzyme is deficient, glucose- 6 - phosphate cannot be converted to glucose. ๏‚ž More glucose is channelled into the HMP shunt, resulting in increased availability of ribose- 5 - phosphate.

๏‚ž This leads to increased formation of PRPP & purine over production. ๏‚ž Elevation of glutathione reductase: ๏‚ž Increased glutathione reductase generates more NADP

which is utilized by HMP shunt. ๏‚ž This causes increased ribose 5 - phosphate & PRPP synthesis