Chapter 17: Citric Acid Cycle Flashcards

(48 cards)

1
Q

is a central pathway for recovering energy from several metabolic fuels, including
carbohydrates, fatty acids, and amino acids, that are broken down to acetyl-CoA for oxidation.

A

citric acid cycle

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2
Q

what does the citric acid cycle oxidize

A

acetyl-CoA to two molecules of CO2

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3
Q

what does the citric acid cycle oxidizes in a manner that conserves what

A

liberated free energy in
the reduced compounds NADH and FADH2

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4
Q

The cycle is named after the
product of its first reaction

A

citrate

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5
Q

One complete round of the citric acid cycle yields

A

two molecules of CO2

three NADH

one FADH2

GTP or ATP

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6
Q

is consumed in the first step of the citric acid cycle is regenerated in the last step of the cycle.

A

oxaloacetate

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7
Q

the citric acid cycle acts as a multistep catalyst that can what

A

oxidize an unlimited number of acetyl groups

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8
Q

In eukaryotes, all the enzymes of the citric acid cycle are located in the

A

mitochondria

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9
Q

all substrates, including what must be generated in the mitochondria or be
transported into mitochondria from the cytosol.

A

NAD+ and GDP

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10
Q

all the products of the citric acid cycle must be consumed where and transported where

A

mitochondria

cytosol.

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11
Q

however, the net effect of each round of the cycle is
the oxidation of

A

one acetyl group to 2 CO2.

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12
Q

Acetyl-CoAis formed from pyruvate through oxidative decarboxylation by a
multienzyme complex named

A

pyruvate dehydrogenase

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13
Q

This complex contains multiple
copies of three enzymes

A

pyruvate dehydrogenase (E1)

dihydrolipoyl transacetylase
(E2)

dihydrolipoyl dehydrogenase (E3)

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14
Q

Decarboxylates pyruvate yielding a hydroxyethyl-tpp carbanion

A

Thiamine pyrophosphate (tpp)

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15
Q

What are advantages of multienzymes:

A
  1. The distance that substrates must diffuse between active sites is minimized, thereby
    enhancing the reaction rate.
  2. The channeling of metabolic intermediates between successive enzymes in a
    metabolic pathway reduces the opportunity for these intermediates to react with other molecules, thereby minimizing side reactions.
  3. The reactions catalyzed by a multienzyme complex can be coordinately controlled.
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16
Q

Accepts the hydroxyethyl carbanion from TPP as an acetyl group

A

Lipoic acid

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17
Q

Accepts the acetyl group from lipoamide

A

Coenzyme A (CoA)

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18
Q

Reduced by lipoamide

A

Flavin adenine

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19
Q

Reduced by FADH2

A

Nicotinamide adenine dinucleotide (NAD+)

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20
Q

acts as a swinging arm

21
Q

what does lipoamide do

A

swings disulfide group from E1 (where it picks up a hydroxyethyl group)

to the E2 active site (where the
hydroxyethyl group is transferred to form acetyl-CoA)

to E3 (where the reduced disulfide is reoxidized)

22
Q

are toxic because they bind to sulfhydryl compounds (including lipoamide) that can form bidentate adducts.

A

arsenite and organic arsenicals

23
Q

The inactivation of lipoamide-containing enzymes by what

24
Q

brings respiration to a halt

A

pyruvate dehydrogenase

25
This differential toxicity is the basis for the early twentieth century use of organic arsenicals in the treatment of
syphilis
26
Aconitase contains a
[4Fe–4S] iron–sulfur cluster
27
that presumably coordinates the OH group of citrate to facilitate its elimination
[4Fe–4S] iron–sulfur cluster
28
normally participate in redox processes
Iron–sulfur clusters
29
The α-ketoglutarate dehydrogenase reaction chemically resembles the reaction catalyzed by
pyruvate dehydrogenase multienzyme complex
30
is the only membrane-bound enzyme of the citric acid cycle
Succinate dehydrogenase
30
catalyzes the stereospecific dehydrogenation of succinate to fumarate
Succinate dehydrogenase
31
In eukaryotes, the products of the pyruvate dehydrogenase reaction, NADH and acetyl-CoA, also activate the
pyruvate dehydrogenase kinase
32
the hormone that signals fuel abundance
Insulin
33
reverses the inactivation by activating pyruvate dehydrogenase phosphatase, which removes the phosphate groups from pyruvate dehydrogenase.
Insulin
34
The citric acid cycle's flux is controlled primarily by three simple mechanisms:
(1) substrate availability (2) product inhibition (3) competitive feedback inhibition by intermediates further along the cycle.
35
Perhaps the most crucial regulators of the citric acid cycle are
its substrates acetyl-CoA and oxaloacetate, and NADH
36
Since the citric acid cycle is a cyclical pathway, any of its intermediates can be converted to oxaloacetate and used for gluconeogenesis.
Gluconeogenesis
37
is a cytosolic process that requires acetyl-CoA. Acetyl-CoA is generated in the mitochondrion but transported across the mitochondrial membrane as citrate
Fatty acid biosynthesis
38
An increase in the concentrations of citric acid cycle intermediates supports increased flux of
acetyl groups through the cycle
39
Pyruvate carboxylase― senses the need for more citric acid cycle intermediates through its activator
acetyl-CoA
40
subsists largely on lipids, using the citric acid cycle to produce precursors for amino acid synthesis and using the glyoxylate cycle to produce carbohydrate precursors.
glyoxylate cycle
41
also stimulates cell growth and differentiation by increasing the synthesis of glycogen, proteins, and triacylglycerols.
Insulin
42
Muscle cells and adipocytes express an insulin-sensitive glucose transporter known as
GLUT4.
43
inhibits transcription of the genes encoding the gluconeogenic enzymes PEP carboxykinase, fructose-1,6-bisphosphatase, and glucose-6-phosphatase and stimulates transcription of the genes for the glycolytic enzymes glucokinase and pyruvate kinase.
Insulin
44
Most of the brain's energy production powers the
plasma membrane
45
which maintains the membrane potential required for nerve impulse transmission.
plasma membrane
46
is the brain's primary fuel.
glucose
47
blood glucose concentration of less than half the normal value of what results in brain dysfunction.
~5 mM