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Chapter-20 Citric Acid Cycle

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 Chapter 20
Citric Acid Cycle

Chapter at a Glance
The learner will be able to answer questions on the following topics:
ˆˆCitric acid cycle ˆˆRegulation of citric acid cycle
ˆˆSignificance of citric acid cycle ˆˆIntegration of metabolism

History: Before 1937, Car Martias, Fray Knoop and Albert

Szent-Gyorgyi had elucidated most of the reactions
described in this chapter. The complete cycle was pro-
posed by Sir Hans Krebs in 1937 (Nobel prize, 1953).
The cycle is there­fore named after him. Please note that
the name is Krebs cycle (there is no apostrophe).
Krebs proposed the original name as TCA (tricarbox-
ylic acid) cycle, beca­use he was not sure whether citric
Fig. 20.1: Sources and utilization of acetyl-CoA
acid is a member of the cycle. Later, Ogston (1948)
showed that the tricarboxylic acid in question is indeed
citric acid, and so the name Citric Acid cycle was given Reactions of the Cycle
later. Scheele in 1780 had isolated citric acid from citrus Preparatory Steps
fruits.
Acetyl-CoA enters the cycle, and is completely oxidized.
During this process, energy is trapped. The sources of
Functions of the Citric Acid Cycle acetyl-CoA are shown in Figure 20.1. Pyruvate derived
1. The final common oxidative pathway that oxidizes from glycolysis is oxidatively decarboxy­lated to acetyl-
acetyl-CoA to CO2. CoA by the pyruvate dehydrogenase (see Fig. 10.19).
2. The source of reduced coenzymes that provide the This is the link between the TCA cycle and glycolysis.
substrate for the respiratory chain. The acetyl-CoA is also derived from beta-oxidation of
3. The link between catabolic and anabolic pathways fatty acids. All the enzymes of citric acid cycle are loca­
(amphibolic role). ted inside the mitochondria.
4. Provides precursors for synthesis of amino acids
and nucleotides.
First Step: Formation of Citric Acid
5. Components of the cycle have a direct or indirect con- The 4 carbon, oxaloacetate condenses with 2 carbon,
trolling effects on key enzymes of other pathways. acetyl-CoA to form 6 carbon compound, the citrate

(tricarboxylic acid). The enzyme is citrate synthase
(step 1, Fig. 20.2). The hydrolysis of the thioester bond
in acetyl-CoA drives the reaction forward. This is an ir-
reversible step. However, body can reverse this step by
another enzyme, ATP-citrate lyase (see Fig. 13.11).
Second Step: Formation of Isocitrate
Citrate is isomerized to isocitrate by aconitase (step 2,
Fig. 20.2). This reaction takes place in two steps, with
cis-aconitate as the intermediary.
Third Step: Formation of
Alpha Ketoglutarate
This reaction is catalyzed by the enzyme, isocitrate
dehydrogenase (step 3, Fig. 20.2). First isocitrate is
dehydrogenated to form oxalosuccinate. It undergoes
spontaneous decarboxylation to form alpha ketoglutar-
ate. The NADH generated in this step is later oxidized
in electron transport chain (ETC) to generate ATPs.
Isocitrate (6 carbons) undergoes oxidative decarboxy-
lation to form alpha ketoglutarate (5 carbons). In this
reaction, one molecule of CO2 is liberated.
Fourth Step: Formation of Succinyl-CoA
Next, alpha ketoglutarate is oxidatively decar­boxy­
lated to form succinyl-CoA by the enzyme alpha keto-
glutarate dehydrogenase (step 4, Fig. 20.2). The
NADH thus generated enters into ETC to generate
ATPs. Another molecule of CO2 is removed in this step.
This is the only irreversible step in the whole reaction
cycle. The enzyme alpha ketoglutarate dehydrogenase
is a multienzyme complex having 3 enzyme proteins
Carl Albert Alexander Hans Adolf
Wilhelm Szent- George Krebs
Scheele Gyorgyi Ogston NP 1953
1742–1789 NP 1937 1911–1996 1900–1981
1893–1986
Chapter 20:  Citric Acid Cycle 329
and 5 coenzymes. This is similar to the pyruvate dehy-
drogenase reaction (Compare Fig. 20.3 with Fig. 10.19).
Fifth Step: Generation of Succinate
The next reaction involves a substrate level phospho-
rylation whereby a high energy phosphate is generated
from the energy trapped in the thioester bond of succinyl-
CoA. The enzyme is succinate thiokinase (step 5, Fig.
20.2). A molecule of GDP is phosphorylated to GTP
and succinate is formed. The GTP can be converted to
ATP by reacting with an ADP molecule:
GTP + ADP → GDP + ATP
Sixth Step: Formation of Fumarate
Succinate is dehydroge­nated to fumarate, an unsatu-
rated dicarboxylic acid, by succinate dehydrogenase
(step 6, Fig. 20.2). The hydrogen atoms are accepted
by FAD. The FADH2 then enters into ETC to generate
ATPs. The succinate dehydrogenase is competitively
inhibited by malonate (see Fig. 5.19).
Seventh Step: Formation of Malate
The formation of malate from fumarate is catalyzed by
fumarase (step 7, Fig. 20.2). The reaction involves the
addition of a water molecule.
Eighth Step: Regeneration
of Oxaloacetate
Finally malate is oxidized to oxaloacetate by malate
dehydrogenase (step 8, Fig. 20.2). The coenzyme is
NAD+. The NADH is generated in this step, which enters
the electron transport chain, when ATPs are produced.
The oxaloacetate can further condense with another
acetyl-CoA molecule and the cycle continues (Fig. 20.2).
Oxaloacetate as a Junction Point
Oxaloacetate may be viewed as a catalyst, which enters
into the reaction, causes complete oxidation of acetyl-
CoA and comes out of it without any change. Oxalo­
acetate is an important junction point in metabolisms. Var-
ious reactions of oxaloacetate are shown in Figure 20.4.
Significance of citric acid cycle is shown in Box 20.1.
330 Textbook of Biochemistry

Fig. 20.2: Krebs cycle or citric acid cycle or tricarboxylic acid cycle

Complete Oxidation of Acetyl-CoA A. Step 3, oxalosuccinate to alpha ketoglutarate

B. Step 4, alpha ketoglutarate to succinyl-CoA (Fig.
CO2 Removal Steps 20.5).
During the citric acid cycle, two carbon dioxide mole- Acetyl-CoA contains 2 carbon atoms. These two
cules are removed in the following reactions: carbon atoms are now removed as CO2 in steps 3 and 4.

Fig. 20.3: Alpha ketoglutarate dehydrogenase reaction; compare
it with Figure 10.19
Box 20.1: Significance of citric acid cycle
1.  Complete oxidation of acetyl-CoA
2.  ATP generation
3.  Final common oxidative pathway
4.  Integration of major metabolic pathways
5.  Fat is burned on the wick of carbohydrates
6.  Excess carbohydrates are converted as neutral fat
7.  No net synthesis of carbohydrates from fat
8.  Carbon skeletons of amino acids finally enter the citric acid
cycle
9.  Amphibolic pathway
10.  Anaplerotic role.
Net result is that acetyl-CoA is completely oxidized
during one turn of cycle.
ATP Generating Steps in TCA Cycle
There are 3 NADH molecules generated during one
cycle, each of them will give rise to 2 ½ ATPs on oxida­
tion by electron transport chain (ETC); so altogether
they will give 3 × 2 ½ = 7 ½ (7.5) high energy phos-
phates. The FADH2 will generate 1½ molecules of ATP.
In addition, one molecule of GTP (equivalent to one mol-
ecule of ATP) is formed by substrate level phospho-
rylation. Hence, per turn of the cycle, 10 high energy
phosphates are produced. These steps are marked in
Figure 20.5 and in Table 20.1. The summary is shown in
Table 20.2.
Chapter 20:  Citric Acid Cycle 331
Fig. 20.4: Reactions of oxaloacetate
Note: Recent work shows that in the electron transport
chain, NADH produces only 2.5 ATPs and FADH only
1.5 ATPs. The old values are also given for comparison
in Table 20.1.
Alpha ketoglutarate dehydrogenase reaction is the
only one irreversible step in the cycle. The free energy
changes of the reactions of the cycle are such that the
cycle will operate spontaneously in the clockwise dire­
ction.
Only about 33% of liberated energy is trapped as
ATP. The rest is used to keep the body temperature at a
higher level than the environment.
Final Common Oxidative Pathway
Citric acid cycle may be considered as the final common
oxidative pathway of all foodstuffs. As shown in Figure
20.9, all the major ingredients of food stuffs are finally
oxidized through the TCA cycle.
Almost all the biochemical processes use ATP for
meeting energy needs—muscle contraction, active trans­
port, biosynthetic reactions, etc. A thermodynamically
unfavo­rable reaction when coupled with hydrolysis of
ATP becomes favorable.
Integration of Major Metabolic Pathways
i. Carbohydrates are metabolized through glycolytic
pathway to pyruvate, then converted to acetyl-CoA,
which enters the citric acid cycle.
ii. Fatty acids through beta-oxidation, are broken
down to acetyl-CoA and then enters this cycle.
iii. Glucogenic amino acids after trans­ amination
enter at some or other points in this cycle (Fig.
20.9). Ketogenic amino acids are converted into
acetyl-CoA.
332 Textbook of Biochemistry

Fig. 20.5: Summary of Krebs citric acid cycle. Enzymes are numbered. Reactions number 3 and 4 are carbon dioxide elimination
steps. Physiological regulatory steps are: Step No.1(citrate synthase) is physiologically inhibited by ATP. Step No.3 (ICDH) is inhibited
by NADH and activated by ADP. Steps where energy is trapped are marked with the coenzyme and the number of ATP generated dur-
ing that reaction. A total of 10 ATPs are generated during one cycle. Recent work shows that in the electron transport chain, NADH may
produce only 2 ½ ATPs and FADH only 1 ½ ATPs

TABLE 20.1: ATP generation steps TABLE 20.2: Stoichiometry of the TCA cycle
Step ATPs (old- ATPs (new Acetyl-CoA            2 CO2 +CoA-SH
No Reactions Coenzyme calculation) calculation) Oxaloacetate            
Oxaloacetate
3 Isocitrate → NADH 3 2.5 FAD               FADH2
alpha ketoglutarate
3NAD+              3 NADH
4 Alpha ketoglutarate NADH 3 2.5
GDP + Pi              GTP
→ succinyl-CoA
5 Succinyl-CoA GTP 1 1
→ Succinate
Fat is Burned on the Wick
6 Succinate → FADH2 2 1.5
Fumarate of Carbohydrates
8 Malate → Oxalo NADH 3 2.5
The oil in a lamp by itself cannot be lighted; the flame
acetate
needs a wick (Fig. 20.6). Similarly in the body, oxida-
Total 12 10
tion of fat (acetyl-CoA) needs the help of oxaloacetate.
One passage of cycle oxidizes acetyl-CoA into two CO2
iv. The integration of metabolism is achieved at junc- molecules. Here oxaloacetate acts as a true catalyst; it
tion points by key metabolites (Fig. 20.9). Several enters the cycle and is regenerated at the end. The major
pathways can converge at this point with the result source of oxaloacetate is pyruvate (carbohydrate).
that carbon atoms from one source can be used for Hence, carbohydrates are absolutely required for oxida-
synthesis of another. Important intermediates are tion of fats, or fats are burned in the fire of carbohy-
pyruvate, acetyl-CoA and oxaloacetate. drates.

Fig. 20.6: Flame needs a wick; oxidation of fat needs carbohydrate
Excess Carbohydrates are
Converted as Triacyl Glycerol
Excess calories are deposited as fat in adipose tissue.
The pathway is glucose to pyruvate to acetyl-CoA to fatty
acid. However, fat cannot be converted to glucose
because pyruvate dehydrogenase reaction (pyruvate
to acetyl-CoA) is an absolutely irreversible step (Fig.
20.7).
No Net Synthesis of
Carbohydrates from Fat
Acetyl-CoA entering in the cycle is completely oxidized
to CO2 by the time the cycle reaches succiny-CoA (see
Fig. 20.2). So, acetyl-CoA is completely broken down in
the cycle. Thus acetyl-CoA cannot be used for gluco­
neogenesis. Therefore, there is no net synthesis of
carbohydrates from fat (Fig. 20.7).
Amino Acids Finally Enter
the TCA Cycle
Some amino acids, such as leucine, catabolized to
acetyl-CoA; are not converted to glucose, because
pyruvate to acetyl-CoA reaction is irreversible. The
acetyl-CoA molecules either enter the TCA cycle and
are completely oxidized, or are channeled to ketone
body formation. Hence, they are called as ketogenic
amino acids (Fig. 20.9). Glucogenic amino acids get
converted to intermediates of TCA cycle.
Amphibolic Pathway
All other pathways, such as beta-oxidation of fat or gly-
cogen synthesis are either catabolic or anabolic. But
Chapter 20:  Citric Acid Cycle 333
Fig. 20.7: Fat cannot be converted to glucose
TCA cycle is truly amphibolic (both catabolic and ana-
bolic) in nature. (Greek, amphi = both). There is a con-
tinuous influx (pouring into) (Fig. 20.9) and a continuous
efflux (removal) of 4-carbon units from the TCA cycle
(Fig. 20.8). In a traffic circle, many roads converge and
traffic flows towards one direction. Since various com-
pounds enter into or leave from TCA cycle, it is some-
times called as “metabolic traffic circle”. Important
anabolic reactions related with citric acid cycle are:
a. Oxaloacetate is the precursor of aspartate
b. Alpha ketogutarate can be made into glutamate
c. Succinyl-CoA is used for synthesis of heme
d. Mitochondrial citrate is transported to cytoplasm,
where it is cleaved into acetyl-CoA, which then is
the starting point of fatty acid synthesis (see Fig.
13.11).
Anaplerotic Role of TCA Cycle
The citric acid cycle acts as a source of precursors of
biosynthe­tic pathways, e.g. heme is synthesized from
succinyl-CoA and aspartate from oxaloacetate. To coun-
terbalance such losses, and to keep the concentrations
of the 4-carbon units in the cell, anaplerotic reactions
are essential. This is called anaplerotic role of TCA cycle
(Greek word, ana = up; plerotikos = to fill). Anaplerotic
reactions are “filling up” reactions or “influx” reactions
or “replenishing” reactions which supply 4-carbon units
to the TCA cycle (Fig. 20.9). The important anaplerotic
reactions are:
a. Pyruvate to oxaloacetate by pyruvate carboxylase
enzyme (see Fig. 10.21). It needs ATP.
b. Glutamate is transaminated to alpha ketogluta­rate;
and aspartate to oxaloacetate. Other important
amino acids entering the TCA cycle are shown in
Figure 20.9.
c. Pyruvate can be carboxylated to malate by NADP+
dependent malic enzyme.
334 Textbook of Biochemistry
Fig. 20.8: Efflux of TCA cycle intermediates
REGULATION OF CITRIC ACID CYCLE
Citrate and Citrate Synthase
The formation of citrate from oxalo acetate and acetyl-
CoA is an important part of control (step 1, Fig. 20.5).
ATP acts as an allosteric inhibitor of citrate syn-
thase. Citrate inhibits PFK (key enzyme of glycolysis);
stimulates fructose-1,6-bisphosphatase, (key enzyme
of gluconeogenesis) and activates acetyl-CoA car­
boxylase (key enzyme of fatty acid synthesis).
Availability and Cellular Need of ATP
When the energy charge of the cell is low, the cycle
operates at a faster rate. The cycle is tightly coupled
to the respiratory chain providing ATP. The Krebs
cycle is the largest generator of ATP among metabolic
pathways.
Anaerobiasis (hypoxia) will inhibit ETC, when
NADH and FADH2 are accumulated, which in turn will
cause inhibition of TCA cycle.
Isocitrate Dehydrogenase
Step 3, (see Fig. 20.5). ADP acts as a positive modifier
enhan­cing the binding of substrate. NADH is an inhibitor.
Fig. 20.9: Influx of TCA cycle intermediates
Alpha Ketoglutarate Dehydrogenase
It is inhibited by succinyl-CoA and NADH.
Regulation of the TCA cycle, like that of glycolysis,
occurs at both the level of entry of substrates into the
cycle as well as at the key reactions of the cycle. Fuel
enters the TCA cycle primarily as acetyl-CoA. The gen-
eration of acetyl-CoA from carbohydrates is, therefore,
a major control point of the cycle. This is the reaction
catalyzed by the PDH complex.
The PDH complex is inhibited by acetyl-CoA and
NADH and activated by nonacetylated CoA (CoASH)
and NAD+. Since three reactions of the TCA cycle as
well as PDH utilize NAD+ as cofactor, the cellular ratio
of NAD+/NADH has a major impact on the flux of carbon
through the TCA cycle.
Citrate inhibits citrate synthase, α-KGDH is inhibited
by NADH and succinyl-CoA. The operation of citric acid
cycle has an obligatory requirement for Thiamine since
both PDH and Alpha KGDH reactions require TPP as
coenzyme.
Inhibitors of TCA Cycle
The above-said mechanisms are physiological and regu­
latory in nature. But the following are toxic or poisonous
 Chapter 20:  Citric Acid Cycle 335

TABLE 20.3: Metabolic defects of oxidative metabolism as a link between catabolic and anabolic pathways
Enzymes Reactions catalyzed Abnormalities (amphibolic role).
Pyruvate Pyruvate → acetyl- Lactic acidosis 2. Citric acid cycle is the source of reduced coen-
dehydrogenase CoA Neurological zymes (that form substrate for respiratory chain)
disorders
as well as precursors for synthesis of proteins and
Acyl-CoA Fatty acyl-CoA Organic aciduria, glutaric
nucleotides (anaplerotic pathway).
dehydrogenase → alpha, beta- aciduria, acidosis,
unsaturated fatty hypoglycemia . Electron 3. The sources of acetyl-CoA are pyruvate (from gly-
acyl-CoA flow from FAD → CoQ colysis) fatty acids (beta-oxidation), and ketogenic
affected
amino acids.
Pyruvate Pyruvate → Oxaloacetate needed
carboxylase Oxaloacetate for sparking TCA cycle is 4. All enzymes of the cycle are located inside the
deficient. Lactic acidosis, mito­chondria.
hyperammonemia and
hyperalaninemia
5. 3 NADH molecules are generated in the cycle at
steps 3, 4 and 8. One FADH2 is formed at steps
6 and one GTP is formed at step 5.
(nonphysiological) agents which inhibit the reactions. 6. Both the carbon atoms of acetyl-CoA are removed
These are shown in Figure 20.5. as CO2 at steps 3 and 4.
A. Aconitase (citrate to aconitate) is inhibited by 7. 10 molecules of ATP are produced per turn of the
fluoroacetate. This is noncompetitive inhibition. TCA cycle (1 FADH2 = 1.5 ATP, 3 NADH = (3 × 2.5=
B. Alpha ketoglutarate dehydrogenase (alpha keto- 7.5 ATP, 1 GTP = 1 ATP). It is the main generator of
glutarate to succinyl-CoA) is inhibited by Arsenite. ATP among metabolic pathways.
This again is noncompetitive inhibition. 8. Alpha ketoglutarate dehydrogenase is the only irre­
C. Succinate dehydrogenase (succinate to fuma- versible step in the TCA cycle.
rate) is inhibited by malonate; this is competitive 9. Oxaloacetate is the true catalyst, which enters and
inhibition. leaves the cycle unchanged.
10. Oxidation of fat (acetyl-CoA) needs help of oxalo­
Metabolic Defects Related to Krebs Cycle acetate whose major source is pyruvate (carbohy-
Though extremely rare, some enzyme deficiency states drates). In other words, fats are burnt in the fire of
have been found to affect the operation of TCA cycle. carbohydrates.
These are given in Table 20.3. 11. Fat cannot be converted to glucose, as pyruvate to
acetyl-CoA is an irreversible step.
LEARNING POINTS, CHAPTER 20 12. The TCA cycle is regulated by cellular need of ATP.
1. Citric acid cycle is the final common oxidative path- 13. Deficiency of pyruvate dehydrogenase causes lac-
way that oxidizes acetyl-CoA to CO2. It also acts tic acidosis and neurological disorders.

PART-1: ESSAY AND SHORT NOTE QUESTIONS

20-1. Discuss the formation of Acetyl-CoA from pyruvate. How is acetyl-CoA is further metabolized in the citric acid
cycle?
20-2. Give an account of the citric acid cycle and explain why it is called the common terminal metabolic pathway.
20-3. Write the steps of Citric Acid Cycle. What is the biological significance of this cycle?
20-4. Describe the reactions of the citric acid cycle. How many ATP molecules are generated per molecule of acetyl-
CoA entering the cycle?
20-5. Explain the amphibolic nature of citric acid cycle.
336 Textbook of Biochemistry
SHORT NOTE QUESTIONS
20-6. Energy releasing steps of citric acid cycle
20-7. Carbon dioxide releasing steps during oxidation of glucose
PART-2: MULTIPLE CHOICE QUESTIONS
20-1. All the enzymes catalyse reactions involving re-
moval of carbon dioxide, except:
A. Alpha ketoglutarate dehydrogenase
B. Glutamate dehydrogenase
C. Pyruvate dehydrogenase
D. Isocitrate dehydrogenase
20-2. Which intermediate of TCA cycle is an unsaturated
dicarboxylic acid?
A. Succinate B. Malate
C. Oxaloacetate D. Fumarate
20-3. Glucose has 6 carbon atoms; these are removed
as carbon dioxide in all the following steps, except:
A. Succinate dehydrogenase reaction
B. Pyruvate dehydrogenase reaction
C. Isocitrate dehydrogenase step
D. Alpha ketoglutarate dehyrogenase step
20-4. How many ATPs are generated per one rota-
tion of the citric acid cycle? (how many ATPs are
produced when one molecule of acetyl-CoA is
oxidised in TCA cycle?)
A. 2 B. 8
C. 10 D. 15
20-5. All the following reactions involve in the genera-
tion of NADH, except:
A. Isocitrate to alpha ketoglutarate
B. Alpha ketoglutarate to succinyl-CoA
C. Fumarate to malate
D. Malate to oxaloacetate
20-6. Acetyl-CoA is used for the production of all the
following, except:
A. Oxidation in TCA cycle
B. De novo synthesis of fatty acid
C. Glucose
D. Cholesterol
20-7. Acetyl-CoA is produced from all the following,
except:
A. Pyruvate
B. Beta-oxidation of fatty acids
C. Leucine
D. Aspartic acid
20-8. Succinyl-CoA is formed from all the following, except:
A. Aspartic acid B. Isoleucine
C. Valine D. Odd chain fatty acids
20-9. Fumarate is produced from all the following,
except:
A. Malate B. Argininosuccinate
C. Phenylalanine D. Tryptophan
20-10. TCA cycle is regulated by the availability of:
A. ATP
B. Glucose
C. Fatty acid
D. Succinate dehydrogenase
20-11. Which is the substrate level phosphorylation step
in the TCA cycle?
A. Alpha ketoglutarate to succinyl-CoA
B. Succinyl-CoA to succinate
C. Succinate to fumarate
D. Malate to oxaloacetate
20-12. During starvation, all the following substances are
increased in blood or tissues, except:
A. Ketone bodies B. Epinephrine
C. Glycogen D. Glucagon
20-13. Which of the following enzymes is confined to the
mitochondria?
A. Lactate dehydrogenase (LDH)
B. Malate dehydrogenase (MDH)
C. Glucose–6-phosphate dehydrogenase
D. Succinate dehydrogenase (SDH)
20-14. Starvation activates all the enzymes, except:
A. Alanine amino transferase
B. Carnitine acyltransferase
C. HMG-CoA lyase
D. ATP citrate lyase
20-15. Which of the coenzymes do not take part in TCA
cycle?
A. NAD+ B. PLP
C. FAD D. TPP
20-16. The amino acids entering TCA cycle as succinyl-
CoA are all except:
A. Valine B. Methionine
C. Tyrosine D. Isoleucine
20-17. Which of the reactions listed replenishes a TCA
cycle intermediate?
A. Heme synthesis
B. Transamination of oxaloacetate
C. Carboxylation of pyruvate
D.
Reutilization of ketone bodies.
 Chapter 20:  Citric Acid Cycle 337

20-18. The TCA cycle is the final common oxidative path-
way because
A. It provides large a fraction of energy
B. Acetyl-CoA derived from all sources can be oxidi­
zed
C. Operates in the mitochondria close to ETC
D. It is a cyclical process
20-19. Which of the intermediates listed is a dicarboxylic
hydroxy acid?
A. Succinate B. Fumarate C. Fluoroacetate and aconitase
C. Malate D. Oxaloacetate
20-20. Which amino acid can enter the TCA cycle as fuma­
rate and oxaloacetate?
A. Aspartate B. Glutamate
C. Arginine D. Serine.
20-21. From the pairs of inhibitors and enzymes, pick out
the mismatched pair.
A. Alpha ketoglutarate dehydrogenase and arsenite
B. Malonate and succinate dehydrogenase
D. Iodoacetate and malate dehydrogenase

ANSWERS OF MULTIPLE CHOICE QUESTIONS

20-1.
B 20-2.
D 20-3.
A 20-4.
C 20-5.
C 20-6.
C 20-7.
D
20-8.
A 20-9.
D 20-10.
A 20-11.
B 20-12.
C 20-13.
D 20-14.
D
20-15. B 20-16.
C 20-17.
C 20-18. B 20-19.
C 20-20.
A 20-21. D

PART-3: VIVA VOCE QUESTIONS AND ANSWERS

20-1. What are the steps in which carbon dioxide is 20-6. How many ATPs are generated per one rotation of
liberated, during oxidation of glucose? the citric acid cycle?
Pyruvate dehydrogenase; Isocitrate dehydrogenase; 10 ATP .
Alpha ketoglutarate dehydrogenase 20-7. What is the net yield of ATP from one molecule of
20-2. Acetyl-CoA is produced from what substrates? glucose in anaerobic glycolysis?
Pyruvate; Fatty acids; ketogenic amino acids 2 ATP.
20-8. What is the net yield of ATP from one molecule of
20-3. Acetyl-CoA is used for what purposes?
glucose in aerobic glycolysis?
Oxidation in TCA cycle; fatty acid synthesis; choles-
7 ATP.
terol synthesis; ketone body formation.
20-9. During complete oxidation, what is the net yield of
20-4. Give examples of substrate level phosphorylation. ATP from one glucose molecule?
1,3-bisphospho glycerate kinase; Pyruvate kinase; 32 ATP.
Succinate thiokinase. 20-10. What is anaplerosis?
20-5. Which is the substrate level phosphorylation step The reactions which involve replenishment of TCA cy-
in the TCA cycle? cle intermediates. For example, pyruvate gives rise to
Succinate thiokinase oxaloacetate.

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