Biochemistry: The Molecular Basis of Life
Biochemistry: The Molecular Basis of Life
6th Edition
ISBN: 9780190209896
Author: Trudy McKee, James R. McKee
Publisher: Oxford University Press
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Chapter 15, Problem 57SA
Summary Introduction

To review:

The end product of the catabolism of the pyrimidine base thymine, the circumstances that lead to excess production of the same, and the reason it does not cause any illnesses, like gout.

Introduction:

Thymine is one of the nitrogenous bases of DNA (deoxyribonucleic acid). In animal cell, she catabolism of these pyrimidine bases occurs through dephosphorylation, deaminatio, nnd the cleavage of the glycosidic bond. The products of pyrimidine catabolism are β-alanine and β-minoisobutyrate. These are further degraded to acetyl CoA (coenzyme A) and succinyl CoA, respectively. Uric acid is the product of purine catabolism.

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Students have asked these similar questions
What is the end product of catabolism of the pyrimidine base thymine? What circumstances cause excess amounts of this end product, and why doesn’t this molecule (unlike uric acid, the end product of purine catabolism) cause a gout-like illness?
What is the end product of catabolism of the pyrimidine basethymine? Unlike uric acid, the end product of purinecatabolism, excess amounts of this molecule do not causeproblems comparable to gout. What circumstances causeexcess amounts of the end product and why doesn’t a goutlike illness result?
why is chymotrypsin inactive at high pH?

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Biochemistry: The Molecular Basis of Life

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