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B.Tech Biotechnology 4th Semester Biochemistry Metabolism.
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๏ The end product of purine metabolism in humans is uric acid. ๏ The nucleotide monophosphates (AMP, IMP & GMP) are converted to their respective nucleoside forms (adenosine, inosine & guanosine) by the action of nucleotidase. ๏ The amino group, either from AMP or adenosine, can be removed to produce IMP or ionosine.
๏ Xanthine oxidase converts hypoxanthine to xanthine & xanthine to uric acid. ๏ This enzyme contains FAD, molybdenum & iron. ๏ It is exclusively found in liver & small intestine. ๏ Xanthine oxidase liberates H2O2 which is harmful to the tissues. ๏ Catalase cleaves H2O2 to H2O & O2.
๏ It is final excretory product of purine metabolism in humans. ๏ Uric acid can serve as an important antioxidant by getting itself converted (non-enzymatically) to allantoin. ๏ It is believed that the antioxidant role of ascorbic acid in primates is replaced by uric acid.
๏ Most animals (other than primates) oxidize uric acid by the enzyme uricase to allantoin, where the purine ring is cleaved. ๏ Allantoin is then converted to allantoic acid & excreted in some fishes. ๏ 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
๏ Hyperuricemia refers to an elevation in the serum uric acid concentration. ๏ This is sometimes associated with increased uric acid excretion (uricosuria).
๏ It is a metabolic disease associated with overproduction of uric acid. ๏ At the physiological pH, uric acid is found in a more soluble form as sodium urate. ๏ In severe hyperuricemia, crystals of sodium urate get deposited in the soft tissues, particularly in the joints. ๏ Such deposits are commonly known as tophi.
๏ PRPP synthetase: ๏ In normal circumstances, PRPP synthetase is under feedback control by purine nucleotides (ADP & GDP). ๏ A variant forms of PRPP synthetase-which are not subjected to feedback regulation-leads to the increased production of purines.
๏ PRPP glutamylamidotransferase: ๏ The lack of feedback control of this enzyme by purine nucleotides also leads to their elevated synthesis. ๏ Deficiency of enzymes of salvage pathway: ๏ HGPRT enzyme of purine salvage pathway & its defect causes Lesch-Nyhan syndrome. ๏ It is associated with increased synthesis of purine nucleotides.
๏ Glucose- 6 - phosphatase deficiency: ๏ This condition is known as von Gierke's disease (glycogen storage disease, type I) ๏ When this enzyme is deficient, glucose- 6 - phosphate cannot be converted to glucose. ๏ More glucose is channelled into the HMP shunt, resulting in increased availability of ribose- 5 - phosphate.
๏ This leads to increased formation of PRPP & purine over production. ๏ Elevation of glutathione reductase: ๏ Increased glutathione reductase generates more NADP
which is utilized by HMP shunt. ๏ This causes increased ribose 5 - phosphate & PRPP synthesis