Discuss the toxic effects of the ammonium ion and excess bicarbonate ion. What is the effect of high concentrations of NH4+ in the bloodstream? What are the two reasons NH4+ is so toxic to the brain? Why can the urea cycle also be considered as a bicarbonate ion disposal mechanism? Why is that important?

Discuss the toxic effects of the ammonium ion and excess bicarbonate ion. What is the effect of high concentrations of NH4+ in the bloodstream? What are the two reasons NH4+ is so toxic to the brain? Why can the urea cycle also be considered as a bicarbonate ion disposal mechanism? Why is that important?

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter10: From Proteins To Phenotypes

Section10.4: Phenylketonuria: A Mutation That Affects An Enzyme

Problem 2GR

See similar textbooks

Similar questions

hyperammonemia in patients is compounded by the reality of the normal regulatory controls in the urea cycle. Explain how increased GDH oxidative deamination activity will inhibit the urea cycle.
What are the energy consuming steps of the urea cycle and what is the energetic cost of the urea cycle in terms of ATP equivalents? How is this cost partially offset and what is the total net cost of the urea cycle?
Which of the following statements regarding the urea cycle is true? (A) Fumarate acts as a connecting link between urea cycle and the CAC.(B) The urea cycle occurs solely in the mitochondria.(C) Citrulline and arginine reacts to form argininosuccinate.(D) Ornithine formed in the last reaction of the urea cycle is excreted from the body along with urea.(E) The purpose of the urea cycle is to produce energy (4 ATP per ammonia that enters) for the liver.
In humans, uric acid is the final product of Allantoin metabolism, Amino acid metabolism, Purine metabolism, or the urea cycle?
Treatments for urea cycle enzyme deficiencies summarize deficiencies and the strategies for treatment.Chose one urea cycle enzyme disorder and describe what are the symptoms and how are the symptoms connected to the mutation? How are the disorder discovered and treated? Is there a dietary approach to treatment and, if so, why does it work? How common is the disorder? Are there populations were incidence more prevalent? And What is the prognosis? (include references)
Including the carbamoyl phosphate synthetase step (CPS I) and the four steps of the urea cycle, how many ATP equivalents (phosphoanhydride bonds) are utilized to drive the formation of one urea molecule?
Production of the enzymes that catalyze the reactions of the urea cycle can increase or decrease according to the metabolic needs of the organism. High levels of these enzymes are associated with high-protein diets as well as starvation. Explain this apparent paradox.
How is the urea cycle linked to the citric acid cycle? Write the net equation of the urea cycle and indicate whether energy is produced or consumed by the cycle. What type of damage occurs if there is a defect in the urea cycle?
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?
What enzyme catalyzes the committed reaction of the urea cycle? carbamoyl phosphate synthetase II carbamoyl phosphate dehydrogenase I carbamoyl phosphate synthetase I carboxyphosphate synthetase II carboxyphosphate synthetase I
Which of the following is a substrate in the urea cycle? a. fumarate b. glutamate c. aspartate d. α-ketoglutarate
Explain how excessive ketone bodies may form in the following: During starvation In patients with diabetes mellitus