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Chapter 07

1. The antibody IgM is produced against any invading microorganism. Ten F ab fragments are
obtained due to the presence of five Y-shaped units of two light and heavy chains each.

2. An immune response occurs when antigen enters an individual’s lymphatic circulation. An injury in
the toe region causes antigens to enter the lymphatic system. However, the swelling in the hip region
is due to the adaptive immune response of lymphatic cells (B cells) to raise specific antibodies against
the antigens.

3. a. ~ 2.6 mm Hg. This can be calculated from any line of data in the table. For example:
P02
Y0 2 =
P50 + P02
0.5
0.161=
x + 0.5
x = 2.6 mm Hg
b. ~ 92 %
P02
Y0 2 =
P50 + P02
30 mm Hg
x=
2.6 mm Hg + 30 mm Hg
x = 0.92 = 92%

4. a. Decrease P 50 .

b. Increase P 50 .

c. Decrease P 50 .

5. a. % Saturation at 100 mm Hg ~98%; % Saturation at 30 mm Hg ~56%

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Chapter 07

b. Percent delivered is the difference between arterial blood (lungs @ P O2 = 100 torr) and venous
blood (tissues @ P O2 = 30 torr).

%Delivered = 98%-56% = 42%

c. Figure 7.27 shows that the % saturation in the capillaries at pH 6.8 is roughly 35%.

Therefore: %Delivered = 98%-35% = 63%

6. a. The concentration of 2, 3-BPG, an allosteric effector, increases within 2 days of moving to a


higher altitude. 2,3-BPG in red cells nearly doubles (from 4.5 mM to ~7.6 mM), which results in
increased binding of this effector to hemoglobin, lowering the oxygen affinity of hemoglobin.

b. This difference in hemoglobin levels is the result of adaptive response to overcome the hypoxic
conditions at high altitudes. Longer-term adaptation to higher altitudes, which requires 2 to 3 months,
is the result of increased red cell production, which is responsible for increased hemoglobin levels.

7. a. Because H146 lies in the α/β interface (see Figure 7.23), mutation should be expected to interfere
with the T � R transition. The effect is to increase affinity. This mutation is known; it is hemoglobin
Hiroshima.

b. Because F8 is involved in heme binding (see Figure 7.25), the heme should be unstable. Leucine
will not ligate to the heme iron.

In each case, a single base change could give rise to the mutation.

8. The anode represents the (+) side of the electric field; thus, molecules with increased (−) charge
density will be more strongly attracted to the anode.

a. Faster because (−) charge density increases for this mutation.

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Chapter 07

b. Probably same, because at pH = 8.0 His is expected to be largely deprotonated (and therefore
uncharged). The Leu side chain in the mutant is aliphatic and uncharged.

9. In general, when an initial protein separation is carried out using column chromatography, proteins
of similar size or shape get separated. It is then possible to identify a specific protein by using the
western blotting technique.

10. a.
 (85)3.2   (25)3.2 
∆YO2 = YO2 (lungs ) − YO2 (capillaries )=  − = 0.961 − 0.334= 0.627
 (31)3.2 + (85)3.2   (31)3.2 + (25)3.2 
 
   

b. Living at 1460 m (~ 4600 ft), the Dalai Lama has adapted to a lower atmospheric P O2 . These
adaptations included elevated [2,3-BPG], which will shift P 50 to higher values.

11. a. Yes, because the linkage between subunits is such that forcing one pair of helices apart favors
moving the other pair apart, making O 2 binding easier in the second pair.

b. Probably. Deprotonation of His 13 destroys the salt bridge, allowing easier opening of the O 2
binding site.

c. The molecule would exhibit higher O 2 affinity and probably lesser cooperativity because the O 2
binding sites would be opened further. Possibly, the whole structure would become unstable.

12. The negative charge on the Asp side chain can form salt bridges with the other (+)-charged side
chains in the BPG–binding pocket and stabilize the T-state. In essence, the Asp side chain is
mimicking the (−) charge on BPG.

13. a. Total length of one thick filament and two thin filaments: 1.5 µm +1 µm +1 µm = 3.5 µm

Length of relaxed sarcomere = 2.3 µm. Thus, total length that must involve overlap: 3.5 µm-2.3 µm =
1.2 µm.

Per thin filament: 1.2 µm/2 = 0.6 µm overlap

When contracted, the total length of sarcomere = 2 µm.

As above: 3.5 µm – 2 µm = 1.5 µm/2 = 0.75 µm overlap

b. Total change in length for a contraction: 2.3 µm – 2 µm = 0.3 µm

Movement in one step 15 nm, or 0.015 µm, which means there must be 20 cycles of 0.015 µm to
account for a movement of 0.3 µm. Since these cycles occur at each end of the thick filament (i.e.,

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Chapter 07

there are two ends at which movement occurs), each end accounts for 10 cycles (or steps) per
contraction.

mol 1L 1mL 1min


14. a. ATP: 4 ×10−3 × × × =
0.0033min or 0.2 sec
L 1000mL 1.2 g 1×10−3 mol

mol 1L 1mL 1min


b. Creatine: 25 ×10−3 × × × =
0.032 min or 1.26 sec
L 1000mL 1.2 g 1×10−3 mol

c. Creatine phosphate must be continually produced in active muscle.

15. a. Release of the myosin headpiece from the thin filament requires ATP binding. Until ATP binds,
the myosin-actin cross-bridge will remain intact, thereby preventing extension of the sarcomeres.

b. Without the action of the Ca2+ transporter, Ca2+ will leak across the membrane from the side of
high Ca2+ concentration (in the transverse tubule) to the side of lower Ca2+ concentration (inside the
sarcomere). As [Ca2+ ] increases, it will bind TnC, thereby stimulating myosin binding to actin. The
lack of ATP will result in a persistent cross-bridge (see part [a]), characteristic of the rigor state.

c. Decomposition includes cleavage of actin and myosin by intracellular proteases (e.g., enzymes
such as trypsin and chymotrypsin described in Chapter 5).

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