BIOCHEMISTRY ANSWERS: tissue is controlled by insulin, which is secreted by the islet

cells of the pancreas in response to an increased

1. D concentration of glucose in the portal blood. In the fasting
2. E state, the glucose transporter of muscle and adipose tissue
3. D (GLUT-4) is in intracellular vesicles. An early response to
4. B insulin is the migration of these vesicles to the cell surface,
5. D where they fuse with the plasma membrane, exposing active
6. A glucose transporters. These insulin-sensitive tissues only take
7. D up glucose from the bloodstream to any significant extent in
8. A the presence of the hormone. As insulin secretion falls in the
9. E fasting state, so that the receptors are internalized again,
10. D reducing glucose uptake.
11. B
12. B 42.Ans. a. GLUT-1.
13. D • Highest level of GLUT1 is present in the RBC
14. E • Major Glucose transporter in brain is GLUT1 (not
15. D present in neurons)
16. D • Major Glucose transporter in the Placenta is GLUT 1
17. D • Major Glucose transporter in the RBC is GLUT1
18. B • Major neuronal Glucose transporter is GLUT3
19. A • Insulin-responsive glucose transporter is GLUT4,
20. D GLUT 8 and GLUT 12
21. B • Fructose transporter GLUT 5 (mainly) and GLUT 11
22. A • Urate transporter is GLUT 9
23. A • Glucose transporter in blastocyst is GLUT 8.
24. D
25. C 43.Ans. a. Hexokinase, Phosphofructokinase, Pyruvate
26. C Kinase
27. A Remember All the Kinases are irreversible except 1,3
28. C Bisphosphoglycerate Kinase which is reversible.
29. C
30. D 44. Ans. a. Glycolysis
31. E In 1924, the biochemist Otto Warburg and his colleagues
32. A made the discovery that cancer cells take up large amounts
33. C of glucose and metabolize it to lactic acid, even in the
34. D presence of oxygen. This observation was termed the
35. D Warburg effect. Based on these data, Warburg made two
36. C hypotheses: first, that the increased ratio of glycolysis to
37. A aerobic respiration was likely due to defects in the
38. E mitochondrial respiratory chain; and second, that this
39 Ans. d. Sugar alcohol. enhanced glycolysis enabled cancer cells to preferentially
• In Diabetes mellitus, in the lens by polyol pathway. Glucose proliferate in the reduced oxygen tension often seen in
converted to Sorbitol by the enzyme Aldose reductase tumors. Furthermore, Warburg argued that the switch
• In galactosemia, Dulcitol or Galactictol is responsible for from aerobic to anaerobic glucose metabolism was the
cataract driver of tumorigenesis.
• Sorbitol, Dulcitol are sugar alcohols
45. Ans. a. Phosphofructokinase
40.Ans. b. Hunter’s Disease Regulatory steps of Glycolysis are
• Hexokinase/Glucokinase
• Phosphofructokinase
• Pyruvate Kinase.
Harper says Phosphofructokinase occupy a key position
in regulating Glycolysis and is also subject to feed back
control.

46. Ans. b. Acetyl CoA

Lactate from muscle and RBC are converted to glucose in
41. Ans. c. Adipocytes the liver (Coris Cycle) Lactate and Alanine is converted to
GLUT-4 and Insulin Glucose uptake into muscle and adipose Pyruvate which can enter into Gluconeogenesis.
Oxaloacetate is converted to Phosphoenolpyruvate by
PEPCK and enter into Gluconeogenesis.
47. Ans. c. Glucose 6 Phosphatase
The answer should be an enzyme common to Glycogenolysis
and Gluconeogenesis
48. Ans. b. Alanine in the liver
Major Substrates for Gluconeogenesis
• Glucogenic Amino Acid (Alanine is the major contributor)
• Lactate
• Glycerol
Propionate (Major contributor in Ruminants).
49. Ans. a. Glucose
• Acetyl CoA is NEVER a substrate for gluconeogenesis
• Acetyl CoA is the starting material for Fatty acid and
Cholesterol synthesis
• Acetyl CoA is an intermediate in Ketone body synthesis.
50. Ans. d. Fatty acid mobilization is low
Glucose-6-phosphatase deficiency leading to hypoglycemia.
Glucose-6-phosphate converted to Pyruvate. This is
converted to Acetyl CoA. As oxaloacetate is depleted because
of using up of Oxaloacetate for Gluconeogenesis, Acetyl CoA
enter in to Ketone body synthesis. Hence Ketosis. Glucose-6-
phosphate also enters into HMP shunt pathway which leads
to more production of Pentoses. Therefore more purine
synthesis. Purines degrade to Uric Acid. Hence there is
Hyperuricemia. As there is hypoglycemia, fat is mobilized.
This also leads to more Acetyl CoA by Fatty acid oxidation.
This increases Ketone body synthesis. Hence Ketosis.
51. Ans. b. Glycogen storage disorder
• Patients with type I GSD may present in the neonatal period
with hypoglycemia and lactic acidosis
• These children often have doll-like faces with fat cheeks,
relatively thin extremities, short stature, and a protuberant
abdomen that is due to massive hepatomegaly; the kidneys
are also enlarged, whereas the spleen and heart are normal
• The biochemical hallmarks of the Type I a GSD (von
Gierke’s) disease are hypoglycemia, lactic acidosis,
hyperuricemia, and hyperlipidemia.
52. Ans. c. Acid maltase
53. Ans. a. More formation of pentoses
Biochemical defect in von Gierke’s
Glucose 6 Phosphatase deficiency → Glucose 6 Phosphate
accumulate → channeled to Pentose Phosphate pathway
→ more Pentoses → To Purine Synthesis → So Uric acid
the degradation product Purine accumulate.
54. Ans. a. Vitamin C
• Uronic acid pathway cannot synthesize Vitamin C in
humans and higher primates because of lack of L-
Gulanolactone Oxidase.
55. Ans. b. Pyruvate Dehydrogenase
In Thiamine deficiency, PDH reaction is defective. So
Pyruvate is converted to lactic acid.
Causes of inhibition of PDH leading to lactic acidosis:
• Inherited PDH deficiency
• Thiamine deficiency
• Alcoholics due to thiamine deficiency
• Arsenite and Mercury poisoning
56. Ans. d. Omega-3 fatty acid.
Significance of ω3 Fatty Acid
• Decrease the risk of Cardiovascular Disease
• Appear to replace arachidonic acid in platelet membranes
• Lower the production of thromboxane and tendency of the
platelet aggregation
• Decrease Serum Triglycerides
• Important for Infant Development
• Lower the risk of various mental illness (Depression, ADHD)
• Lower the risk of chronic degenerative diseases such as
Cancer, Rheumatoid Arthritis, and Alzheimers Disease.
57. Ans. a. Glucocerebroside.

Gaucher’s Disease
• Most common Lysosomal Storage Disorder
• Glucocerebrosidase defect
• Lysosomes filled with Glucocerebroside
• No cherry red spot in the macula
• No mental deterioration (Type I)
• Hematological features: Pancytopenia, bleeding
manifestation
• Hepatosplenomegaly
• Bone Pain and Pathological Fractures of long bones
• X-ray Femur Erlenmeyer Flask Deformity
• Bone Marrow Biopsy Gaucher cell with Wrinkled paper
appearance/crumbled tissue paper appearance
58. Ans. c. Niemann-Pick Disease.
Niemann-Pick Disease Autosomal Recessive Biochemical
defect
• Deficient activity of acid sphingomyelinase, a
lysosomal enzyme encoded by a gene on chromosome
11
• Accumulation of sphingomyelin and other lipids in the
monocyte-macrophage system.
Clinical features
• Failure to thrive
• Hepatosplenomegaly
• Rapidly progressive neurodegenerative course.
Treatment
• Orthotopic liver transplantation
• Amniotic cell transplantation
• Bone marrow transplantation
• Miglustat
• A phase I trial of enzyme replacement therapy for type B
NPD.
59. Answer B: Linoleic is an essential fatty acid in that it must
be acquired in the diet. Linoleic acid is especially important in
that it required for the synthesis of arachidonic acid.
Arachidonate is a precursor for the eicosanoids (the
prostaglandins, thromboxanes, and leukotrienes). It is this
role of linoleic acid in eicosanoid synthesis that leads to poor
growth, wound healing, and dermatitis in persons on fat-free
diets
60. Answer A: The major building block for the synthesis of
TGs, in tissues other than adipose tissue, is glycerol. The
glycerol backbone of TG is activated by phosphorylation at
the sn3 position by glycerol kinase
61. Answer C: Platelet-activating factor (PAF) is a unique
complex lipid of the plasmalogen family. PAF functions in
hypersensitivity, acute inflammatory reactions, and
anaphylactic shock by increased vasopermeability,
vasodilation, and bronchoconstriction. Excess production of
PAF production may be involved in the morbidity associated
with toxic shock syndrome and strokes.
62. Answer B: Glucocerebrosides are only intermediates in
the synthesis of complex gangliosides or are found at
elevated levels only in disease states such as Gaucher
disease, where there is a defect in the catabolism of the
complex
gangliosides. Thus, the presence of high concentrations of
glucocerebrosides in cells such as monocytes and
macrophages is indicative of a metabolic defect.
63. Answer E: Infants with Tay-Sachs disease appear normal
at birth. Symptoms usually begin with mild motor weakness
by 3 to 5 months of age. Parents will begin to notice that
their afflicted child has a dull response to outside stimuli.
Another early symptom is an exaggerated startle response.
By 6 to 10 months of age infants will begin to show
regression of prior acquired motor and mental skills. It is the
loss of these activities that will normally prompt parents to
seek a medical opinion. A progressive loss in visual
attentiveness may lead to an ophthalmological consultation
which will reveal macular pallor and the presence of the
characteristic “cherry-red spot” on the fundus of the eye.
64. Answer B: Gaucher disease is characterized by the
lysosomal accumulation of glucosylceramide
(glucocerebroside) which is a normal intermediate in the
catabolism of globosides and gangliosides. Gaucher disease
results from defects in the gene encoding the lysosomal
hydrolase: acid β-glucosidase, also called glucocerebrosidase
The hallmark feature of Gaucher disease is the presence of
lipid-engorged cells of the monocyte/macrophage lineage
with a characteristic appearance in a variety of tissues. These
distinctive cells contain one or more nuclei and their
cytoplasm contains a striated tubular pattern described as
“wrinkled tissue paper.” These cells are called Gaucher cells
65. Answer C: Nonsteroidal anti-inflammatory drugs inhibit
cyclooxygenase and consequently inhibit (not promote,
choice E) synthesis of prostaglandins. In the stomach,
prostaglandins have a cytoprotective effect through
inhibition of acid secretion, enhancement of mucosal blood
flow, and stimulation of bicarbonate and mucus secretion.
Inhibiting these processes can cause stomach ulcers and
bleeding such as described in the case.
66. Answer C: Due to the vasodilating action of PGE1, it is
used pharmaceutically as alprostadil to treat newborn infants
with ductal-dependent congenital heart disease. The
administration of alprostadil in these infants maintains a
patent ductus arteriosus until surgery can be carried out to
correct the underlying heart defect. Ductus arteriosus is a
normal structure of the fetal heart that allows blood to
bypass circulation to the lungs since the fetus does not use
his/her lungs in utero. The ductus arteriosus shunts blood
flow from the left pulmonary artery to the aorta. Shortly after
birth, the ductus closes due to the high levels of oxygen the
newborn is exposed to at birth. However, in newborns with
certain congenital heart defects, maintaining a
patent ductus arteriosus is clinically significant.
67. Answer D: The antipyretic (fever reducing) effects of
aspirin are due to the ability of this drug to block the
synthesis of pro-inflammatory and pyretic prostaglandins
from arachidonic acid. The synthesis of the prostaglandins is
initiated via the activity of PGS. This enzyme possesses 2
activities, COX and peroxidase. One of the actions of aspirin
(acetylsalicylic acid) is the inhibition of the COX activity of
PGS.
68. Answer B: Oxidation of fatty acids occurs in the
mitochondria and the peroxisomes via similar enzymatic
pathways referred to as β-oxidation. Fatty acids of between 4
and 8 and between 6 and 12 carbon atoms in length, referred
to as short- and medium-chain fatty acids (SCFAs and
MCFAs), respectively, are oxidized exclusively in the
mitochondria. Long-chain fatty acids (LCFAs: 10-16 carbons
long) are oxidized in both the mitochondria and the
peroxisomes with the peroxisomes exhibiting preference for
14-carbon and longer LCFAs. Very-longchain fatty acids
(VLCFAs: 17-26 carbons long) are exclusively oxidized in the
peroxisomes.
69. Answer D: In infants, the supply of glycogen lasts less
than 6 hours and gluconeogenesis is not sufficient to
maintain adequate blood glucose levels. Normally, during
periods of fasting (in particular during the night) the
oxidation of fatty acids provides the necessary ATP to fuel
hepatic gluconeogenesis as well as ketone bodies for
nonhepatic tissue energy production. In patients with MCAD
deficiency there is a drastically reduced capacity to oxidize
fatty acids. This leads to an increase in glucose usage with
concomitant hypoglycemia. The deficit in the energy
production from fatty acid oxidation, necessary for the liver
to use other carbon sources, such as glycerol and amino
acids, for gluconeogenesis further exacerbates the
hypoglycemia. Normally, hypoglycemia is accompanied by an
increase in ketone formation from the increased oxidation of
fatty acids. In MCAD deficiency there is a reduced level of
fatty acid oxidation, hence near-normal levels of ketones are
detected in the serum.
70. Answer D: Refsum disease is the result of defects in the
oxidation of phytanic acid, a lipid requiring an α-oxidation
pathway. As a consequence phytanic acid accumulates in the
blood and tissues. The hallmark symptoms of the disease are
retinitis pigmentosa, cerebellar ataxia, chronic
polyneuropathy, and an elevation in protein in the
cerebrospinal fluid with no increase in cell count.
71. Answer D: Ketone bodies are synthesized in the liver from
acetyl-CoA. Acetyl- CoA can be derived from the oxidation of
pyruvate, certain amino acids, and fatty acids. By far, the
largest concentration of acetyl-CoA is derived from the β-
oxidation of fatty acids.
72. Answer E: Ketone bodies are synthesized in the liver from
acetyl-CoA. Acetyl- CoA can be derived from the oxidation of
pyruvate, certain amino acids, and fatty
acids. By far, the largest concentration of acetyl-CoA is
derived from the β- oxidation of fatty acids such as palmitic
acid.
73. Answer D: During periods of fasting and starvation the
liver diverts acetyl- CoA, derived from the oxidation of amino
acids and fatty acids, into ketogenesis. The ketone bodies,
acetoacetate and β-hydroxybutyrate, produced by the liver
are then delivered to the blood and oxidized by peripheral
tissues, such as the brain, for ATP production.
74. Answer D: When cells cannot effectively oxidize fatty acid,
or are in need of storage fat, the fats are diverted into
triglyceride synthesis. In an individual with a defect in
carnitine synthesis, or a dietary carnitine deficiency, fatty acid
oxidation will be impaired resulting in the diversion of the
fats into triglycerides.
75. Answer A: During the pathway of fatty acid oxidation the
molecules are first activated by attachment of CoA
generating a fatty acyl-CoA derivative. The fatty acyl-CoA
derivatives are then substrates for the enzyme carnitine
palmitoyltransferase I, which substitutes carnitine for CoA
generating a fatty acylcarnitine which can then be
transported across the outer mitochondrial membrane.
76. Answer B: HMG-CoA reductase is the rate-limiting
enzyme of cholesterol biosynthesis and the major site for
regulation of this metabolic pathway. Regulation
of HMGR through covalent modification occurs as a result of
phosphorylation and dephosphorylation. The enzyme is most
active in its unmodified form. Phosphorylation of the enzyme
decreases its activity. HMGR is phosphorylated by AMPK,
which itself is activated via phosphorylation. Increased AMPK
activity would, therefore, have a significant negative impact
on the rate of HMGR activity
77. Answer C: Cholestyramine is a drug belonging to the bile-
binding resin class of cholesterol-lowering drugs. These drugs
function by binding bile acids in the gut, thereby, preventing
their reuptake. Inhibition of bile acid uptake into the
enterohepatic circulation will result in increased bile salt
concentrations in the feces, including deoxycholate, a
primary bile salt.
78. Answer B: Nicotinic acid, derived from niacin, reduces the
plasma levels of both VLDLs and LDLs by inhibiting hepatic
VLDL secretion, as well as suppressing
the flux of FFA release from adipose tissue by inhibiting
lipolysis. In addition, nicotinic administration strongly
increases the circulating levels of HDLs. Patient
compliance with nicotinic acid administration is sometimes
compromised because of the unpleasant side effect of
flushing (strong cutaneous vasodilation).
79. Answer E: The cellular uptake of cholesterol from LDL
occurs following the interaction of LDL with the LDL receptor
(also called the apoB-100/apoE receptor). Both apoB-100,
which is exclusively associated with LDL, and apoE are
required for LDL receptor-mediated endocytosis of LDL. The
importance of apoE in cholesterol uptake by LDL receptors
has been demonstrated in transgenic mice lacking functional
apoE genes. These mice develop severe atherosclerotic
lesions at 10 weeks of age. Therefore, increased levels of
apoE would be associated with a higher hepatic uptake of
LDL, leading to reduced levels in the blood.
80. Answer D: Smith-Lemli-Opitz syndrome (SLOS) is an
autosomal recessive disorder resulting from a defect in
cholesterol synthesis. The defect resides in the terminal
enzyme of the cholesterol biosynthesis pathway, namely 7-
dehydrocholesterol reductase. Defects in this gene result in
increased levels of 7- dehydrocholesterol and reduced levels
(15%-27% of normal) of cholesterol in SLOS patients. The
clinical spectrum of SLOS is very broad, ranging from the
most severe form manifesting as a lethal malformation
syndrome, to a relatively mild disorder that encompasses
behavioral and learning disabilities. A frequent observation in
SLOS infants is poor feeding and postnatal growth failure.
There are distinct craniofacial anomalies associated with
SLOS, which include microcephaly (head size smaller than
normal), micrognathia (abnormally small lower jaw), ptosis
(drooping eyelids), a small upturned nose, and cleft palate or
bifid uvula. Male infants with SLOS exhibit genital
abnormalities that range from a small penis to ambiguous
genitalia or gender reversal. Abnormalities in limb
development are common in SLOS patients and include short
thumbs, postaxial polydactyly, and single palmar creases. In
addition, the most common clinical finding in SLOS patients is
syndactyly (fusion of digits) of the second and third toes. This
latter limb deformity is found in over 95% of SLOS patients.
81. Answer B: Chylomicrons are assembled in the intestinal
mucosa as a means to transport dietary cholesterol and
triglycerides to the rest of the body. The apolipoproteins that
predominate before the chylomicrons enter the circulation
include apoB-48, apoA-I, apoA-II, and apoA-IV, where apoB-
48 is exclusively associated with chylomicrons.
82. Answer B: Chylomicrons are assembled in the intestinal
mucosa as a means to transport dietary cholesterol and
triglycerides to the rest of the body. Chylomicrons leave the
intestine via the lymphatic system and enter the circulation
at the left subclavian vein. High levels of chylomicrons in the
blood can give it a milky appearance. The term chyle refers to
the milky fluid consisting of lymph and emulsified fats or free
fatty acids, which is how the term chylomicron was derived.
83. Answer E: The liver takes up LDL (and IDL) after they have
interacted with the LDL receptor to form a complex, which is
endocytosed by the cell. For LDL receptors in the liver to
recognize LDL, they require the presence of both apoB-100
and apoE (the LDL receptor is also called the apoB-100/apoE
receptor). Lack of functional LDL receptors is associated with
hypercholesterolemia and the increased
development of atherosclerotic plaques, leading to coronary
heart disease.
84. Answer B: Chylomicrons are assembled in the intestinal
mucosa as a means to transport dietary cholesterol and
triglycerides to the rest of the body. Chylomicrons are,
therefore, the molecules formed to mobilize dietary
(exogenous) lipids. Failure to produce chylomicrons would,
therefore, lead to impaired absorption of dietary lipids.
85. Answer A: The dietary intake of both fat and
carbohydrate, in excess of the needs of the body, leads to
their conversion into triglycerides in the liver. These
triglycerides are packaged into VLDL and released into the
circulation for delivery to the various tissues (primarily
muscle and adipose tissue) for storage or production of
energy through oxidation. VLDL are, therefore, the molecules
formed to transport endogenously derived triglycerides to
extrahepatic tissues. The fatty acid portion of VLDL is
released to the tissues through the action of lipoprotein
lipase, which leads to increasing density of VLDL to IDL and
LDL.
86. Answer E: Hepatic triglycerides are packaged into VLDL
and released into the circulation for delivery to the various
tissues (primarily muscle and adipose tissue) for storage or
production of energy through oxidation. VLDL are, therefore,
the molecules formed to transport endogenously derived
triglycerides to extra-hepatic tissues.
87. Answer D: Major reactions that involve the regulation of
plasma pH as well as the level of circulating ammonia involve
the hepatic and renal enzymes glutamate dehydrogenase
(GDH), glutamine synthase (GS), and glutaminase. The liver
compartmentalizes GS and glutaminase in order to control
the flow of ammonia into glutamine or urea. Under acidotic
conditions the liver diverts ammonia to glutamine via the GS
reaction. The glutamine then enters the circulation. In fact,
glutamine is the major amino acid of the circulation and its
role is to ferry ammonia to and from various tissues. In the
kidneys, glutamine is hydrolyzed by glutaminase (yielding
glutamate) releasing the ammonia to the urine. There the
ammonia ionizes to ammonium ion, NH4 +, which reduces
the circulating concentration of hydrogen ion resulting in an
increase in the pH. Additionally, the glutamate can be
converted to α- ketoglutarate yielding another mole of
ammonia, which is ionized by hydrogen ions further
increasing the pH.
88.Answer A: Seemingly normal full-term infants suffering
from urea cycle defects will usually become lethargic and
need stimulation to feed within 24–72 hours after
birth. When presented in the emergency many will be
comatose. One obvious outward clinical sign will be a bulging
fontanel due to the ammonia-induced encephalopathy. If a
correct diagnosis of hyperammonemia is not made in a timely
manner these infants will die.
89.Answer A: Unlike fats and carbohydrates, nitrogen has no
designated storage depots in the body. Since the half-life of
many proteins is short (on the order of hours), increased
dietary intake of protein will result in an concomitant
increase in amino acid degradation resulting in increased
nitrogen excretion. When more nitrogen is excreted than is
incorporated into the body, an individual is in negative
nitrogen balance. Normal, healthy adults are generally in
nitrogen balance, with intake and excretion being very well
matched. Young growing children, adults recovering from
major illness, and pregnant women are often in positive
nitrogen balance. Their intake of nitrogen exceeds their loss
as net protein synthesis proceeds.
90.Answer C: The dominant reactions involved in removing
amino acid nitrogen from the body are known as
transaminations. Transaminations involve moving an α-
amino group from a donor α-amino acid to the keto carbon
of an acceptor α-keto acid. These reversible reactions are
catalyzed by a group of intracellular enzymes known as
aminotransferases, which generally employ covalently bound
pyridoxal phosphate as a cofactor.
91.Answer B: A deficiency in carbamoyl phosphate
synthetase I is reflective of a urea cycle disorder. A common
thread to most UCDs is hyperammonemia leading to
ammonia intoxication
92.Answer A: The symptoms exhibited by the infant are
reflective of maple syrup urine disease (MSUD). This disease
is caused by defects in branched-chain α-keto acid
dehydrogenase, one of the enzymes used in the catabolism
of the branched-chain amino acids (BCAAs) and the
associated branched-chain α-keto acids (BCKAs).
The classical symptom of this disease is the odor of burnt
sugar in the diapers of afflicted infants. Left untreated,
infants will die in the first few months of life from
recurrent metabolic crisis and neurologic deterioration.
93.Answer C: Histamine is a preformed inflammatory
mediator found principally in mast cells and basophils that
has a major role in the early vascular changes of
inflammation, that is, dilation of precapillary arterioles, which
produces the local redness (rubor) and warmth (calor), and
the increased permeability of postcapillary venules, which
produces the swelling (tumor).
94. Answer E: A deficiency in phenylalanine hydroxylase
(PAH) is the cause of PKU. Tyrosine is produced in cells by
hydroxylating the essential amino acid phenylalanine and this
reaction is catalyzed by PAH. Half of the phenylalanine
required goes into the production of tyrosine; if the diet is
rich in tyrosine itself, the requirements for phenylalanine are
reduced by about 50%.
95. Answer B: The side chain of cysteine contains a reactive
sulfur that can become oxidized, forming intermolecular
disulfide bonds. Exposure of cysteine to air, such as could be
the case in highly oxygen-rich tissue like erythrocytes, can
result in oxidation of the sulfur.
96. Answer E: Albinism is a congenital disorder characterized
by the complete or partial absence of pigment in the skin,
hair, and eyes due to absence or defect of tyrosinase.
Tyrosinase is responsible for the conversion of tyrosine to the
skin pigment melanin.
97. Answer D: Essential amino acids are so-called because
they cannot be synthesized at all or in adequate amounts to
serve the needs of the body. Of the amino acids listed, only
methionine is an essential amino acid and is thus likely to be
present in the leaves of the desert trees.
98. Answer E: In cardiac and skeletal muscle, high-energy
phosphate is stored through the transfer of a phosphate from
ATP to creatine generating creatine phosphate. Creatine is
synthesized in liver from guanidoacetate. Guanidoacetate is
derived from the amino acid arginine in the kidneys. In
muscle cells, creatinine is a nonenzymatic metabolite of
creatine phosphate. When measured in the serum, levels
of creatinine are remarkably constant from day to day and
are proportional to muscle mass. In renal dysfunction, the
clearance of creatinine will be impaired and its levels will
therefore rise in the serum. Although creatine is synthesized
in the liver from guanidoacetate, which is produced in the
kidney, it is not used by these 2 tissues. Once synthesized,
creatine is transported to cardiac and skeletal muscle
where it is phosphorylated and stored for future energy
needs.
99. Answer A: Tetrahydrofolate (THF) is regenerated from the
dihydrofolate (DHF) product of the thymidylate synthase
reaction by the action of dihydrofolate reductase
(DHFR). Cells that are unable to regenerate THF suffer
defective DNA synthesis and eventual death. Many
anticancer drugs act directly to inhibit thymidylate
synthase, or indirectly, by inhibiting DHFR. Many DHFR
inhibitors have been synthesized, including methotrexate,
aminopterin, and trimethoprim. Each of these is an analog of
folic acid
100. Answer A: Synthesis of the pyrimidines requires 1 mole
of glutamine, 1 mole of ATP, and 1 mole of CO2 (which form
carbamoyl phosphate) and 1 mole of aspartate. An additional
mole of glutamine and ATP are required in the conversion of
UTP to CTP.
Alyssa - <50
Gevera - <50
Balasa - <50
Montemayor - <50
Uy- 49
Arcenal - <50
Bernardo - <50
Jiff- 53
Bello - <50
Silot - 51
Abrar - 57
Togado - 52
Acebedo - <50
Poblador - 59
Blancia - 51
Geraldoy - 54
Palanca - 53
Rosas - <50
Daday - <50
Bautista - 49
Bandiola - 58
Gabrinez - 55
Habaradas - 62
Obsioma - 55
Tabujara - <50
Diaz - <50
Cawaling - <50
Abelarde - 59
Dumanon - <50
Gaviola - <50