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Match the metabolic pathway in Figure:17.7 with the reactions listed on 394.

Match the metabolic pathway in Figure:17.7 with the reactions listed on 394.

Biochemistry
Biochemistry
6th Edition
ISBN:9781305577206
Author:Reginald H. Garrett, Charles M. Grisham
Publisher:Reginald H. Garrett, Charles M. Grisham
Chapter31: Completing The Protein Life Cycle: Folding, Processing, And Degradation
Section: Chapter Questions
Problem 8P
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Match the metabolic pathway in Figure:17.7 with the reactions listed on 394.
Chapter 17 : METABOLISM OF NUCLEOTIDES 393 AMP deaminase AMP IMP GMP NH3 H20- H2O- Nucleotidase Nucleotidase Pit Nucleotidase Pit Pit NH2 Adenosine deaminase HN HN H20 NH N' H2N Řibose Řibose Ribose Adenosine Inosine Guanosine PiN Purine nucleoside Ribose + phosphorylase I-phosphate Pi Purine nucleoside phosphorylase HN Ribose 1-phosphate Нурохanthine H20 + O2 Xanthine oxidase HN Guanase HN NH, HO H2N° N. Guanine Xanthine H2O + O2 Хan oxidase H2O, HN N. Uric acid Fig. 17.7 : Degradation of purine nucleotides to uric acid (AMP-Adenosine monophosphate; IMP-Inosine monophosphate; GMP-Guanosine monophosphate).
Transcribed Image Text:Chapter 17 : METABOLISM OF NUCLEOTIDES 393 AMP deaminase AMP IMP GMP NH3 H20- H2O- Nucleotidase Nucleotidase Pit Nucleotidase Pit Pit NH2 Adenosine deaminase HN HN H20 NH N' H2N Řibose Řibose Ribose Adenosine Inosine Guanosine PiN Purine nucleoside Ribose + phosphorylase I-phosphate Pi Purine nucleoside phosphorylase HN Ribose 1-phosphate Нурохanthine H20 + O2 Xanthine oxidase HN Guanase HN NH, HO H2N° N. Guanine Xanthine H2O + O2 Хan oxidase H2O, HN N. Uric acid Fig. 17.7 : Degradation of purine nucleotides to uric acid (AMP-Adenosine monophosphate; IMP-Inosine monophosphate; GMP-Guanosine monophosphate).
394 BIOCHEMISTRY Uric acid Most animals (other than primates) however, oxidize uric acid by the enzyme uricase to allantoin, where the purine ring is cleaved. Allantoin is then converted to allantoic acid and Uricase Allantoin excreted in some fishes (Fig.17.8). Further degradation of allantoic acid may occur to produce urea (in amphibians, most fishes and some molluscs) and, later, to ammonia (in marine invertebrates). Allantoinase Allantoic acid Glyoxylate Allantoicase Urea Urease Ammonia DISORDERS OF PURINE METABOLISM Fig. 17.8 : Degradation of uric acid in animals other than man. Hyperuricemia and gout Uric acid is the end product of purine humans. 1. The nucleotide monophosphates (AMP, metabolism IMP and GMP) are converted to their respective concentration of uric acid in the serum of adults nucleoside forms (adenosine, inosine and guanosine) by the action of nucleotidase. in The normal is in the range of 3-7 mg/dl. In women, it is slightly lower (by about 1 mg) than in men. The daily excretion of uric acid is about 500-700 mg. 2. The amino group, either from AMP or adenosine, can be removed to produce IMP or inosine, respectively. Hyperuricemia refers to an elevation in the serum uric acid concentration. This is sometimes associated with increased uric acid excretion 3. Inosine and guanosine are, respectively, (uricosuria). converted to hypoxanthine and guanine (purine bases) by purine nucleoside phosphorylase. overproduction of uric acid. At the physiological Adenosine is not degraded by this enzyme, pH, uric acid is found in a more soluble form as Gout is a metabolic disease associated with sodium urate. In severe hyperuricemia, crystals of sodium urate get deposited in the soft tissues, hence it has to be converted to inosine. 4. Guanine undergoes deamination by particularly in the joints. Such deposits are guanase to form xanthine. commonly known as tophi. This causes 5. Xanthine oxidase is an important enzyme inflammation in the joints resulting in a painful that converts hypoxanthine to xanthine, and gouty arthritis. Sodium urate and/or uric acid xanthine to uric acid. This enzyme contains may also precipitate in kidneys and ureters that FAD, molybdenum and iron, and is exclusively results in renal damage and stone formation. Historically, gout was found to be often associated with high living, over-eating and tissues. Catalase cleaves H2O2 to H2O and O2. alcohol consumption. In the previous centuries, found in liver and small intestine. Xanthine oxidase liberates H,O2 which is harmful to the Uric acid (2,6,8-trioxypurine) is the final alcohol was contaminated with lead during its excretory product of purine metabolism in humans. Uric acid can serve as an important antioxidant by getting itself converted (non- excretion causing gout. In general, a diet rich is enzymatically) to allantoin. It is believed that the antioxidant role of ascorbic acid in primates is replaced by uric acid, since these animals have lost the ability to synthesize ascorbic acid. manufacture and storage. Lead poisoning leads to kidney damage and decreased uric acid meat and seafoods is associated with increased risk of gout. The prevalence of gout is about 3 per 1,000 persons, mostly affecting males. Post-menopausal
Transcribed Image Text:394 BIOCHEMISTRY Uric acid Most animals (other than primates) however, oxidize uric acid by the enzyme uricase to allantoin, where the purine ring is cleaved. Allantoin is then converted to allantoic acid and Uricase Allantoin excreted in some fishes (Fig.17.8). Further degradation of allantoic acid may occur to produce urea (in amphibians, most fishes and some molluscs) and, later, to ammonia (in marine invertebrates). Allantoinase Allantoic acid Glyoxylate Allantoicase Urea Urease Ammonia DISORDERS OF PURINE METABOLISM Fig. 17.8 : Degradation of uric acid in animals other than man. Hyperuricemia and gout Uric acid is the end product of purine humans. 1. The nucleotide monophosphates (AMP, metabolism IMP and GMP) are converted to their respective concentration of uric acid in the serum of adults nucleoside forms (adenosine, inosine and guanosine) by the action of nucleotidase. in The normal is in the range of 3-7 mg/dl. In women, it is slightly lower (by about 1 mg) than in men. The daily excretion of uric acid is about 500-700 mg. 2. The amino group, either from AMP or adenosine, can be removed to produce IMP or inosine, respectively. Hyperuricemia refers to an elevation in the serum uric acid concentration. This is sometimes associated with increased uric acid excretion 3. Inosine and guanosine are, respectively, (uricosuria). converted to hypoxanthine and guanine (purine bases) by purine nucleoside phosphorylase. overproduction of uric acid. At the physiological Adenosine is not degraded by this enzyme, pH, uric acid is found in a more soluble form as Gout is a metabolic disease associated with sodium urate. In severe hyperuricemia, crystals of sodium urate get deposited in the soft tissues, hence it has to be converted to inosine. 4. Guanine undergoes deamination by particularly in the joints. Such deposits are guanase to form xanthine. commonly known as tophi. This causes 5. Xanthine oxidase is an important enzyme inflammation in the joints resulting in a painful that converts hypoxanthine to xanthine, and gouty arthritis. Sodium urate and/or uric acid xanthine to uric acid. This enzyme contains may also precipitate in kidneys and ureters that FAD, molybdenum and iron, and is exclusively results in renal damage and stone formation. Historically, gout was found to be often associated with high living, over-eating and tissues. Catalase cleaves H2O2 to H2O and O2. alcohol consumption. In the previous centuries, found in liver and small intestine. Xanthine oxidase liberates H,O2 which is harmful to the Uric acid (2,6,8-trioxypurine) is the final alcohol was contaminated with lead during its excretory product of purine metabolism in humans. Uric acid can serve as an important antioxidant by getting itself converted (non- excretion causing gout. In general, a diet rich is enzymatically) to allantoin. It is believed that the antioxidant role of ascorbic acid in primates is replaced by uric acid, since these animals have lost the ability to synthesize ascorbic acid. manufacture and storage. Lead poisoning leads to kidney damage and decreased uric acid meat and seafoods is associated with increased risk of gout. The prevalence of gout is about 3 per 1,000 persons, mostly affecting males. Post-menopausal
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