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Chapter 13: Problem 1

(a) The citric acid cycle converts one molecule of citrate to one molecule of oxaloacetate, which is required for the cycle to continue. If other cycle intermediates are depleted by being used as precursors for amino acid biosynthesis, can a net synthesis of oxaloacetate occur from acetyl CoA via the enzymes of the citric acid cycle? (b) How can the cycle continue to function if insufficient oxaloacetate is present?

Short Answer

Expert verified
a) No, a net synthesis of Oxaloacetate from Acetyl CoA via the cycle cannot occur if cycle intermediates are depleted. b) The cycle can continue to function even if insufficient Oxaloacetate is present through anaplerotic reactions, which refill the cycle by reforming Oxaloacetate.

Step by step solution

01

Understanding the Citric Acid Cycle

The citric acid cycle starts with Acetyl-CoA combining with Oxaloacetate to form Citrate. The cycle ends by oxidizing the intermediates into the initial component Oxaloacetate and thereby allowing the cycle to start again. Importantly, in the Citric Acid Cycle, Oxaloacetate is regenerated in each turn of the cycle, meaning it acts as a catalyst.
02

Synthesis of Oxaloacetate

In response to the first question, if intermediates of the cycle are used up to synthesize amino acids, a net synthesis of Oxaloacetate from Acetyl CoA via the cycle cannot occur. This is because the Citric Acid Cycle is a closed loop: the Oxaloacetate needed to initiate the cycle is regenerated by the end of the cycle.
03

Functioning with Insufficient Oxaloacetate

Regarding the second question, if insufficient Oxaloacetate is present, the cycle can be replenished using a process called anaplerotic reactions. These reactions refill the cycle by reforming Oxaloacetate. They can either convert Pyruvate or other components into Oxaloacetate through carboxylation reactions or rearrange the atoms in existing cycle intermediates using transaminase reactions.

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Most popular questions from this chapter

Pyruvate dehydrogenase complex deficiency is a disease that results in various metabolic and neurological effects. Pyruvate dehydrogenase complex deficiency can cause lactic acidosis in affected children. Other clinical symptoms include increased concentrations of pyruvate and alanine in the blood. Explain the increase in the levels of pyruvate, lactate, and alanine in individuals with pyruvate dehydrogenase complex deficiency.

The activities of PFK-2 and fructose 2,6-bisphosphatase are contained in a bifunctional protein that effects tight control over glycolysis and gluconeogenesis through the action of fructose 2,6-bisphosphate. Describe another protein that contains kinase and phosphatase activities in a single protein molecule. What pathways does it control?

(a) How many molecules of ATP are generated when two molecules of acetyl CoA are converted to four molecules of \(\mathrm{CO}_{2}\) via the citric acid cycle? How many molecules of ATP are generated when two molecules of acetyl CoA are converted to oxaloacetate in the glyoxylate cycle? (b) How do the yields of ATP relate to the primary functions of the two pathways?

A deficiency of a citric acid cycle enzyme in both mitochondria and the cytosol of some tissues (e.g., blood lymphocytes) results in severe neurological abnormalities in newborns. The disease is characterized by excretion in the urine of abnormally large amounts of \(\alpha\)-ketoglutarate, succinate, and fumarate. What enzyme deficiency would lead to these symptoms?

Calculate the number of ATP molecules generated by the following net reactions of the citric acid cycle. Assume that all \(\mathrm{NADH}\) and \(\mathrm{QH}_{2}\) are oxidized to yield ATP, pyruvate is converted to acetyl \(\mathrm{CoA}\), and the malate-aspartate shuttle is operating. (a) 1 Pyruvate \(\longrightarrow 3 \mathrm{CO}_{2}\) (b) Citrate \(\longrightarrow\) Oxaloacetate \(+2 \mathrm{CO}_{2}\)
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