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Chapter 28 Review Question Answers
1.
a. The fat-soluble vitamins are vitamin A, vitamin D, vitamin E, and vitamin
K.
b. The water-soluble vitamins are vitamin C, thiamine (Β1), riboflavin (Β2),
niacin (B3), pantothenic acid (B5), vitamin B6, biotin (B7), folic acid (B9).
and vitamin B12.
c. The B-complex vitamins are thiamine (Β1), riboflavin (Β2), niacin (B3),
pantothenic acid (B5), vitamin B6, biotin (B7), folic acid (B9), and vitamin
B12.
2.
a. Enrichment is the process of replacing vitamins that are lost during the
processing of a food to approximate their original levels.
b. Fortification is the process of adding vitamins to food, during or after
processing, to increase the level above that naturally found in the food.
3.
a. Most vitamins function as cofactors for enzymes.
b. Vitamin A and vitamin D function as hormones.
4.
a. Vitamin A, in the form of retinal, is involved in the chemistry of vision in
the rod cells of the retina. Deficiencies result in an inability to see in dim
light (night blindness). Vitamin A, in the form of retinoic acid, is involved
in the proper maintenance of cellular differentiation of the cornea and
conjuntival mucosa. Deficiencies lead to corneal and conjunctival
thickening and eventually to corneal necrosis, which can lead to
permanent blindness.
b. Retinoic acid would not be the proper treatment for a deficiency of this
vitamin. Retinoic acid is not involved in vision but only in cellular
differentiation. Furthermore, it cannot be converted in vivo into retinal,
which is the form required for vision.
c. Forms of vitamin A that would supply retinol must be used, such as the
vitamin As or provitamin A carotenoids, since both retinal and retinoic
acid can be formed from these sources in vivo. (See Figures 28.1 and 28.4
for more detail.)
5.
There is limited absorption and bioconversion in the intestine of the
provitamin A carotenoids, which apparently limits the amount converted to
active vitamin A, even with high doses of the provitamin A carotenoids.
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6.
a. Cholecalciferol, one of the active forms of Vitamin D, can be synthesized
from cholesterol in the skin upon exposure to adequate sunlight. Vitamin
D becomes a vitamin only with limited exposure of the skin to sunlight or
sunlight of inadequate intensity.
b. The active nucleotide form of niacin can be synthesized from the amino
acid tryptophan; however, the conversion is generally too inefficient to
supply the complete niacin requirement unless the diet is abnormally high
in tryptophan.
7.
a. The enzyme 7-dehydrocholesterol reductase reduces cholesterol to
produce 7-dehydrocholesterol. In the skin, exposure to UV radiation
(sunlight) in the range of 290 to 300 nm results in rapid conversion of 7dehydrocholesterol to previtamin D3. Previtamin D3 undergoes slow
thermal conversion to cholecalciferol (vitamin D3) and to the biologically
inactive lumisterol and tacalciol. (See Figure 28.7 for structures.)
b. Excess exposure to sunlight does not produce toxic levels of
cholecalciferol; rather, it increases production of the inactive compounds.
Lumisterol and tacalciol can be converted back to previtamin D3 and thus
serve as a reservoir.
8.
a. The eight members of the vitamin E family, four tocopherols and four
tocotrienols, are known as tocols. Tocols possess two important structural
components, the chromanol ring and the side chain. They differ by the
methylation patterns of the chromanol ring (α-, β-, γ-, and δ-) and the
presence or absence of double bonds in the side chain (no double bond in
tocopherols; three double bonds in tocotrienols).
b. All the tocols are equally absorbed from the intestine. α-Tocopherol enters
the circulation, where it is found in much higher levels than the other
tocols, even though the other tocols predominate in the diet. This
difference is attributed to a liver cytosolic binding protein, α-tocopherol
transfer protein (α-TTP) that is selective for α-tocopherol. Circulating
tocopherols are also carried by α-TTP, which preferentially incorporates
the α-tocopherol into blood low-density lipoproteins (LDLs).
9.
Biotin and pantothenic acid
10.
Severe thiamine deficiency results in Wernicke's encephalopathy or
Wernicke-Korsakoff syndrome in alcoholics and requires immediate therapy
with thiamine.
11.
The failure of vitamin E supplements to demonstrate protective effects against
heart diseases may be due to the fact that they contain only α-tocopherol. To
effectively remove the peroxide damage in these cells by electrophilic
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peroxynitrites or other mutagens, γ-tocopherol is also needed. In addition to
forming the orthoquinone, γ-tocopherol acts in vivo as a trap for these
membrane soluble electrophilic mutagens, forming stable adducts through the
nucleophilic C5, which is blocked in α-tocopherol. (See Figure 28.13 for
detailed structures.) It has been suggested that because α-tocopherol
supplementation suppresses γ-tocopherol levels, a combination of the two
tocopherols in the ratios found in the diet may be more useful than αtocopherol alone.
12.
Renal calculi due to oxalate or urate result from enhanced renal excretion of
these compounds in the presence of high doses of vitamin C. (See Figure
28.49 for the chemical mechanism.) Increased release of calcium and
phosphorus from bone have been observed. Hematological effects include
increased absorption of nonheme iron without significant increases in total
body iron stores. Diarrhea, likely resulting from an osmotic effect, has been
reported following large doses, and ascorbic acid tablets that lodge in the
esophagus can cause local erosion.
13.
a. Vitamin K is required by the enzyme γ-glutamyl carboxylase (Figure
28.19) to form γ-carboxyglutamate (Gla) residues from glutamate on the
vitamin K–dependent proteins to form active proteins. Vitamin K
functions, in conjunction with γ-glutamyl carboxylase, to form a strong
base to extract a proton from the glutamate γ carbon, allowing the γcarboxylation of glutamate by CO2.
b. The known biochemical roles of the Gla proteins are (1) formation of the
procoagulation factors VII, IX, X, and prothrombin, (2) formation of the
anticoagulation factors protein S, protein C, and protein Z, (3) formation
of bone Gla protein and matrix Gla protein in bone and other tissues that
regulate mineralization, and (4) formation of growth arrest-specific 6,
which has effects in cellular proliferation.
14.
Vitamin D and vitamin K both play a role in the proper maintenance of bone
mineralization. Remember, many other factors also play a role.
15.
The active form of folates in vivo is the tetrahydrofolate form, which is
formed by the action of DHFR on those folates in the oxidized state such as
folic acid. Since folic acid requires conversion by DHFR to the
tetrahydrofolate form to be active, and since this is the step inhibited by
methotrexate, folic acid cannot effectively treat the overdose. Leucovorin is
already in the tetrahydrofolate form that does not require bioactivation by
DHFR to enter into the reduced folate pool in the body, so it can act
immediately to provide reduced folate for methyl transfer reactions, thereby
circumventing the action of methotrexate and reducing its toxic effects. (See
Figures 28.43 and 28.44.)
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16.
If the megaloblastic anemia is due to folic acid deficiency, then there is no
harm; however, if the megaloblastic anemia is due to a vitamin B12 deficiency,
which can also cause this form of anemia, then administering folic acid would
reverse the anemia but allow the nerve damage caused by B12 deficiency to
continue unabated. This could lead to a poor outcome. For this reason, the
cause of the anemia needs to be determined first and therapy instituted with
the appropriate vitamin. Of course, there are other causes of this form of
anemia not related to folic acid or vitamin B12 deficiency in which cases
neither vitamin may be appropriate.
17.
a. The purpose of fortification of food with folic acid is to prevent neural
tube defects in pregnancy.
b. All enriched cereal-grain products (flour, rice, bread, rolls, buns, pasta,
corn, grits, cornmeal, farina, macaroni, and noodle products) require
fortification.
18.
a. Niacin has proven effective in the treatment of hyperlipidemias. Niacin, in
high doses, can lower LDL cholesterol and triglycerides and raise HDL
cholesterol.
b. Niacinamide, though as effective as niacin for vitamin therapy, is not
effective in the treatment of hyperlipidemias. Therefore, this would not be
a suitable substitution.
19.
a. Pyridoxal phosphate is the major coenzyme form of vitamin B6.
b. 4-Pyridoxic acid is the inactive form of vitamin B6 that is excreted in the
urine.
c. Pyridoxine, pyridoxal, and pyridoxamine and their corresponding 5'phosphate derivatives, referred to as pyridoxine 5’-phosphate, pyridoxal
5'-phosphate, and pyridoxamine 5'-phosphate. (See Figure 28.34 for
detail). Because of their ability to interconvert, all are considered active
forms of vitamin B6 in vivo.
d. Aldolases, aminotransferases, racemases, and decarboxylases. (See Figure
28.36.)
20.
a. Pernicious anemia is an autoimmune disorder that results in parietal cell
destruction. This results in insufficient production of gastric acid and
intrinsic factor and the ensuing malabsorption of cobalamin. This leads to
a megaloblastic anemia and neurological damage as a result of the vitamin
B12 deficiency.
b. Cyanocobalamin is the form most commonly used because of its high
stability. It is converted into the active hydroxocobalamin in vivo by
cyanocobalamin reductase.
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c. Hydroxocobalamin should be used in two situations. First, it should be
used in the case of a rare genetic disorder of cyanocobalamin reductase
that results in an inability to convert cyanocobalamin to
hydroxocobalamin in vivo. Second, hydroxocobalamin, but not
cyanocobalamin, must be used in the treatment of cyanide toxicity.
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