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BIO-CHEM MODULE 4 EXAM QUESTIONS WITH VERIFIED CORRECT ANSWERS
"Understand the role of high-energy phosphate bonds in ATP (and other nucleotide triphosphates) in the transfer of free energy from exergonic to endergonic processes, enabling
them to act as the energy currency of cells. - CORRECT ANSWER ATP has high phosphoryl
transfer potential that is an intermediate among biologically important phosphorylated molecules compounds derived from this metabolism of fuel power ATP synthesis, and in turn, ATP donates a phosphoryl group to other biomolecules to facilitate their metabolism ATP constantly regenerated via oxidation of carbon in fuel like glucose and fats" "Explain how unfavorable reactions may be driven forward by either high substrate or low product concentrations. Given the deltaG' and the concentrations of substrate and product, be
able to determine if a reaction can proceed spontaneously. - CORRECT ANSWER cells couple
energetically unfavorable reactions to energetically favorable ones to drive overall forward deltaG' = -RT lin [B]/[A] = -RT ln Keq IF G < 0 , then [B] > [A] (Keq > 1) then proceeds forward IF G' > 0, then [A] > [B] (Keq < 1) then proceeds reverse"
"Explain how oxygen consumption is coupled to total body energy expenditure. - CORRECT
ANSWER anaerobic glycolysis can proceed in absense of oxygen only producing 2 ATP instead of
oxidation of glucose through oxidative phosphorylation (30-32 ATPs) ATP is consumed within 60 seconds of generation for energy utlization (muscle contraction, ion transport, biosynthesis, etc) to be regenerated post translational and allosteric regulation (seconds/minutes) --> post transcriptional regulation (hours) --> transcriptional regulation (days)"
"ATP hydrolysis - CORRECT ANSWER energy changes = electrostatic repulsion (phosphates
repel each other), Mg+2 coordination (makes phosphorus more electrophilic), resonance stabilization or stabilization due to hydration (water can bind better to ADP than ATP) -- this results in donation of Pi ATP not expended through hydrolysis bc hydrolysis has high energy of activation (ATPase helps overcome) -Arginine finger helps?
Dont store all energy as ATP bc hydrolyzed too easy and short half-life --> solved by stored in form of creatine phosphokinase (CPK) -- quick energy source in muscle" "Describe the 10 reactions of glycolysis and the energy yield, as well as how its regulation insures cellular ATP homeostasis. KNOW THE 3 IRREVERSIBLE AND HIGHLY REGULATED REACTIONS OF GLYCOLYSIS
(hexo/glucokinase, PFK-1, and pyruvate kinase) - CORRECT ANSWER ENERGY INVESTMENT
PHASE
- Phosphorylation of glucose by hexokinase -- IRREVERSIBLE
- Isomerization (converts aldose to ketose)
- Second phosphorylation of Fructose-6P (PFK-1) -- IRREVERSIBLE, FIRST COMMITTED STEP, RATE LIMITING
- Cleavage of F1,6BP into two 3-carbon molecules (aldolase)
- Isomerization of DHAP to GAP ENERGY GENERATION PHASE
- Oxidation of G3-P to 1,3-BPG (achieved through oxidation-phos reactions)
- Phosphorylation of ADP to syntehsize 3-phosphoglycerate
- Mutase shifts phosphate from C3 to C
- Dehydration of 2-phosphoglycerate by Enolase
- Phosphorylation of ADP using pyruvate kinase, giving pyruvate -2nd set of ATPs is generated here --IRREVERSIBLE uses 2 ATP per glucose, yields 4 ATP and 2 NADH SO only yields 2 ATP total" "Distinguish between tissues that rely wholly, partially, or conditionally upon anaerobic glycolysis and why. What is the connection of anaerobic glycolysis to lactic acid production?
Cori Cycle. - CORRECT ANSWER erythrocytes (RBCs) --> completely dependent on glycolysis
for ATP - no mitochondria anaerobic glycolysis = total amount of NAD+ & NADH is very low, so NADH must be rapidly oxidized for glycolysis to continue // NADH is ocidized to NAD+ by lactade dehydrogenase, only produces 2ATPs/glucose good during short, intense exercise, replenishes very quickly and is 100x faster than oxidative phosphorylation
bypasses the three irreversible steps of glycolysis glucose is synthesized, ATP consumed, NADH is oxidized to NAD+ -starts in mitochondria with pyruvate, uses pyruvate carboxylase & PEP carboxykinase, F16BP- ase, and G-6P-ase, to synthesize glucose (-6 ATP equivalent) -- not exactly the reverse of glycolysis bc have some common enzymes Fructose 2,6-BP reciprocally regulates glycolysis and gluconeogenesis (lowered in fasting, activates GN and favors F6P // raised in well fed state, blocking F16 and thus GL)" "Describe why the enzymatic defect in patients with Hereditary Fructose Intolerance (HFI, Aldolase B deficiency) results in hypoglycemia and lactic acidosis, and what common sources of
sugar HFI patients should avoid? - CORRECT ANSWER Hereditary Fructose Intolerance =
deficiency in aldolase B causes Fructose 1-P to accumulate and intracellular Pi & ATP levels to fall --> decreased ATP compromises gluconeogenesis and liver protein production --> AMP accumulates and is degraded leads to hypoglycemia, hyperuricemia, and liver failure should avoid fructose and sucrose from the diet" "Describe Galactose metabolism (occurs in all tissues, especially liver) and the causes and
consequences of classical and nonclassical galactosemia. - CORRECT ANSWER galactokinase
produces galactose 1-P UDP-galactose is produced in an exchange reaction with UDP-glucose, but can also be converted to UDP-glucose classical galactosemia = accumulation of galactose 1-phosphate and galactitol in nerve, lens, liver, and kidney tissue causes liver damage severe mental retardation and cartaracts for galactokinase deficiency and aldose reductase = elevated galactitol can cause cataracts" "Realize the prevalence of G-6P dehydrogenase deficiency in hemolytic anemia and how oxidative stress (consumption of Fava Beans, primaquine) causes RBC lysis (failure to regenerate Glutathione)
In RBC's, the PPP is the only way NADPH is generated. Other anti-oxidants (vitamin E, C, and
catalase help out in absence of additional oxidative stress. - CORRECT ANSWER deficiency of
G6PD causes hemolytic anemia bc of inability to detoxify oxidizing agents (due to insufficient reduced glutathione) --affects RBCs the most bc only make NADPH via PPP so more severe oxidative stress causes RBC lysis --> oxidant drugs, favism (oxidizing agents like fava beans), and infection (from oxidants produced during infammation) deficiency in G6PD confers evolutionary advantage in some circumstances -- prevalent in Africans bc protects against malaria (parasites require NADPH, and PPP is compromised to parasites die) --> primaquine is a antimalarial drug that will cause hemolysis in individuals deficient in G6PD" "Describe the clinical features of severe thiamine deficiency, and connect the symptoms to the
biochemical role of thiamine in the PDH complex and TCA cycle - CORRECT ANSWER thiamine
deficiency = Beriberi -symptoms include weight loss, emotional disturbances, tremors, lactic acidosis drinking heavily causes poor absorption and storage of thiamine, coenzyme TPP no longer works"
"Describe the biochemical bases of arsenite and fluoroacetate poisoning - CORRECT ANSWER
Arsenite = inhibits pyruvate dehydrogenase complex by inactivating dihydrolipoamide component of transacetylase --reduces overall energy production but can be solved by 2,3-dimercaptopropanol Fluoroacetate = inhibits aconitase (cannot isomerize citrate to isocitrate), results in citrate accumulation -- found in rat poison" "Know that FA synthesis occurs primarily in the liver, and to a lesser extent in adipose. Describe the conversion of excess carbohydrate and protein into cytosolic acetyl-CoA, how this process is regulated, and how it helps to provide some of the cytosolic NADPH necessary for FA
synthesis. - CORRECT ANSWER FA occurs mostly in liver (little in adipose), and is synthesized
from acetyl CoA from excess protein and carbs uses ATP and NADPH, requires lots of acetyl CoA, involves citrate shuttle and is when citrate concentration in mitochondria is high due to inhibition of isocitrate dehydrogenase by high levels of ATP
"Understand the hormonal induction of Fatty acid release and utilization. Describe the transport of FA into mitochondria and diseases that result from defects associated with carnitine involving
CPT I and CPT II. - CORRECT ANSWER transport of FA-CoA derivatives into mitochondria for
oxidation needs carnitine --amine from Lysine and Met, made in liver and kidneys, stored in skeletal muscle CPT = carnitine palmitoyl transferase CPT1 or CPT II deficiency = hypoglycemia, hypoketosis, myoglobinuria -hypoglycermia results from impaired FA oxidation bc steps of gluconeogenesis use NADH and ATP that come from FA oxidation --not enough to allow ketone body synthesis, which impedes gluconeogenesis" "Describe the pathway of mitochondrial B-oxidation, the products that result, the energy yield,
and how this process is regulated. - CORRECT ANSWER 1) oxidation
-FA-CoA is to trans enoyl CoA by dehydrogenase
- hydration -water enters and makes it L-B-hydroxyacyl CoA
- oxidation
- NAD+ comes and takes H+ to make ketoacyl CpA
- thiolysis -CoASH and thioase makes acetyl-CoA results in ATP and more fatty acyl-CoA -for odd cahined ones, proceeds using B oxidation until only propionyl CoA remains regulation -amount of FA is by hormonse -CPT1 is inhibited by malonyl CoA -AMP signals low energy and turns off FA synthesis -NADH/FAD2H build up if not used by Ox-PHOS" "Describe the synthesis of Ketone bodies and how their synthesis is regulated. Know why children are more susceptible than adults to developing ketosis and why are type I diabetics
prone to developing ketoacidosis. Why can't the liver use ketone bodies? - CORRECT ANSWER
During starvation, Acetyl-CoA generated from FA metabolism is converted to ketone bodies -- driven by thiolase, acetoacetyl Coa, and 3-hydroxy-3-methyl glutaryl CoA (HMG CoA) in starvation, brain starts to use ketone bodies to spare glucose --> liver does not have thiophorase and cannot use the ketone bodies it uses
adults are prone to develop ketosis bc the fasting state is reached faster in kids (high muscle/adipose ratio), and so there is less insulin in kids and no malonyl CoA leading to unrestricted entry of FAs into liver and conversion to ketones"
Oxidation of the carbon farthest from the carbonyl group of a fatty acid is called - CORRECT
ANSWER w-oxidation"
"Inorganic nitrogen is initially assimilated into which of the following amino acids - CORRECT
ANSWER Glutamine"
"Glycerol from the hydrolysis of triacylglycerols is transported by the blood to the ____ -
CORRECT ANSWER Liver"
"The intermediates in fatty acid synthesis are linked through a ________linkage to ACP. -
CORRECT ANSWER Thioester"
"How many FADH2 molecules would be produced in the oxidation of palmitic acid (16:
carbons)? - CORRECT ANSWER 7"
"What is the major mechanistic difference in purine and pyrimidine biosynthesis? - CORRECT
ANSWER Purines are synthesized on the ring of ribose"
"The fixation of nitrogen requires _______. - CORRECT ANSWER Fe-Mo protein,
Fe protein, Ferredoxin" "All of the following are purine bases except _____. Guanine, Thymine, Adenine,
Hypoxanthine - CORRECT ANSWER Thymine"
"Which of the following is not a function of lipids: Energy storage, Components of biological membranes, Insulation,
Source of acetyl-CoA - CORRECT ANSWER All of the above are functions of lipids"
"The rate limiting step in fatty acid synthesis is - CORRECT ANSWER Acetyl-CoA
carboxylation"
"Prostaglandins are involved in _________. - CORRECT ANSWER Ovulation,
Inflammation, Digestion"
"Saturated fatty acids containing up to 16 carbon atoms are assembled in ________. - CORRECT
ANSWER Cytoplasm"
"Membrane proteins are linked to anchor molecules through a ___________ link - CORRECT
ANSWER Ether"
"The principal means of producing glycerol in the body - CORRECT ANSWER
Glyceroneogenesis"
"w-6 Fatty acids - CORRECT ANSWER Have a double bond six carbon atoms from the methyl
end of the chain"
"Asparagine is formed from aspartic acid and _________. - CORRECT ANSWER Glutamine"
"All of the following statements concerning folic acid are true except: - CORRECT ANSWER
Folic acid requires intrinsic factor for its absorption in the intestine."
"Energy requiring transport mechanisms include - CORRECT ANSWER Primary active
transport"
most common organic molecule - CORRECT ANSWER glucose"
"how is glucose made - CORRECT ANSWER photosynthesis"
"what happens during photosynthesis - CORRECT ANSWER CO2 and H2O are converted into
starch, cellulose and other plant products"
"glucose formula - CORRECT ANSWER C6H12O6"
"carb formula - CORRECT ANSWER Cn H2n On"
"monosaccharides - CORRECT ANSWER simple sugars"
"oligosaccharides - CORRECT ANSWER short chains of amino acids"
"polysaccharides - CORRECT ANSWER long chains of 20/more monosaccharides"
"polysaccharides can be - CORRECT ANSWER linear or branched"
"carb functions - CORRECT ANSWER energy source, intermediates on metabolic pathways,
structure, and role in DNA and RNA"
"monosaccharides have either a - CORRECT ANSWER aldose or ketose functional group"
"how many carbons do monosaccharides typically have - CORRECT ANSWER 3-8"
"what are the three carbon trioses - CORRECT ANSWER glyceraldehyde and
dihydroxyacetone"
"smallest monosaccharide has - CORRECT ANSWER 3 carbons (trioses)"
"Fischer projection formulas - CORRECT ANSWER 2D structures that represent 3D carbs"
"what carbon is closest to the functional group - CORRECT ANSWER 1"
"Aldose monosaccharides - CORRECT ANSWER Found in 3-6 carbons in length"
"D structure - CORRECT ANSWER OH group is on the right"
"L structure - CORRECT ANSWER OH group is on the left"
"What does D stand for - CORRECT ANSWER dextrorotatory"
"Is glucose D or L - CORRECT ANSWER D"
"What does L stand for - CORRECT ANSWER levorotatory"
"What determines a configuration of a monosaccharide - CORRECT ANSWER The penultimate
carbon, second to last"
"Epimers - CORRECT ANSWER Monosaccharides that differ in the orientation at only 1
position"
carboxylic acid is the most oxidized out of the choices"
"thioester bonds (acetyl-CoA) higher in energy than ordinary esters - CORRECT ANSWER
thioester bond = high energy bond = acetyl coa larger atomic size of S educes overlap (no resonance stabilization) // thioester more unstable relative to ester so releases more energy on hydrolysis" "Describe the breakdown of starch to glucose and the import of glucose by the intestinal
epithelium (SGLT1). - CORRECT ANSWER Starch is broken down by salivary a-amylase and
then pancreatic a-amylase, which catalyze hydrolysis of a(1-4) glycosidic bonds and produce a- maltose, a-isomaltose, and trisaccharides maltose and isomaltose are broken down by maltase and isomaltase into glucose on border of intestinal epithelial cells SGLT1 (sodium-glucose linked transporter 1) which is present on border of intestinal epithelial cells is a symporter and transports glucose & galactose against concentration gradient using energy from gradient of Na+"
"Describe the roles of different glucose transporters (GLUT) - CORRECT ANSWER GLUT2 is a
facilitated glucose transporter that helps glucose travel down its concentration gradient on the other side (high capacity/Vmax, low affinity/high Km) --> gets glucose from SGLT1 in liver, pancreas, and intestine and send to capillaries -insulin independent GLUT5 is a facilitated fructose transporter present on the apical border (inside) GLUT4 is an insulin dependent facilitated glucose transporter, works in muscle and adipose -insulin stimulates movement of GLUT4 to plasma membrane from intracellular vesicles"
"Describe the metabolites derived from glucose and the intermediates/products of glycolysis. -
CORRECT ANSWER Nucleic acid and NADPH synthesis = from 5C sugars from G6P
Triglyceride synthesis = uses glycerol-P and FA (from Acetyl CoA) to make triglycerides, important bc lack glycerol kinase 2,3-BPG = major reaction pathway for consumption of glucose in erythocytes is needed to control Hb affinity for O2" "Explain the biochemical basis of the hemolytic anemia observed in deficiency of erythrocyte
pryuvate kinase, triosephosphate isomerase, and enolase. - CORRECT ANSWER pyruvate
kinase deficiency is second most common cause of anemia --> enzyme with abnormal
properties/kinetics (enzyme activity & stability altered, decreased, or show abnormal Km/Vmax) this results in premature death and lysis of RBCs triosephosphate isomerase = deficiency rare but results in it, accompanied by elevation of DHAP levels in erythrocytes (can't isomerize to G3P) enolase = deficiency is rare, but can cause it (catalyzes dehydration of 2-PG to create phosphoenol pyruvate with high transfer potential) --> no more high potential = premature death"
"Explain the basis of the Warburg effect and how this can be used to locate cancer cells. -
CORRECT ANSWER tumor cells tend to carry out glycolysis at a much higher rate than normal
tissue even when oxygen is available (bypassing oxidative phosphorylation) -p53 tumor suppressor is mutated and defective in electron transport so relies on glycolysis for ATP production // achieved by increased synthesis of hexokinase underlies basis for PET scans (Fluorodeoxyglucose/FdG is administered to look for high glucose metabolizing tissues bc PFK-1 is blocked by it)"
"Glycolysis - CORRECT ANSWER occurs in cytoplasm in ALL cell types
is what RBC's and other cells without mitochondria rely upon for energy production inability to carry this out results in hemolytic anemia"
"Enzyme kinetics of hexokinase vs. glucokinase. - CORRECT ANSWER phosphorylation of
glucose by hexokinase I is an irreversible & regulatory step / feedback inhibited by G6P
- low Km and Vmax, high curve glucokinase = hexokinase iv, expressed in hepatocytes (liver) and pancreatic B cells //regulated indirectly by GKRP to decrease futile cycling bt glucose and G6P under low glu conditions & the lag bt rise in intracellular glu and onset of phosphorylation -high Km and Vmax, lower sloping curve" "Discuss the various sources of carbon substrates for gluconeogenesis. Evaluate the relative
importance of different precursors for gluconeogenesis in feeding, fasting, and exercise. -
CORRECT ANSWER from RBCs, skin, brain, and muscle (Cori Cycle) = lactate dehydrogenase
-- low insulin, high glucagon and FA from degradation of muscle proteins (only good for several days, generally preserved for end) = alanine aminotransferase -- low insulin, high glucagon & FA from degradation of triacylglycerides in adipose tissue (hormone sensitive lipase is activated by glucagon, epinephrine, and cortisol) = glycerol kinase / glycerol 3-phosphate dehydrogenase
- Glucose 6-P is converted into 6-phosphoglucono-lactone catalyzed by G6PD (glucose 6- phosphate dehydrogenase) -- generates NADPH, which inhibits G6PD
- 6-phosphogluconolactone hydrolase converts it to 6-phosphogluconate -irreversible
- 6-phosphogluconate is oxidatively decarboxylated to ribulose 5-phosphate via 6- phosphogluconate dehydrogenase -- produces NADPH and CO
- ribulose 5-phosphate isomerase and ribulose 5-phosphate epimerase ?? occurs in all cell types, only pathway for generation of NADPH in cells without mitochondria --sudden increase in PPP activity is fastest known response to oxidative stress by generating NADPH"
"Describe the role of Xylulose 5-phosphate in carbohydrate & FA metabolism. - CORRECT
ANSWER excess carb (and insulin) results in liver making lipids in the form of TAG
glycose influx causes increased Xu-5-P, and this activates protein phosphatase 2A (PP2A) PP2A dephosphorylates and activates ChREBP (carb response element bp), causing nuclear translocation and INCREASING LIPID Synthesis"
"transketolase - CORRECT ANSWER can convert ribulose-5-P into glyceraldehyde-3-P and
fructose-6-P to create NADPH TPP is a cofactor for transketolase can be used to assay thiamine deficiency --> measurement is done in absence and presence of exogenous TPP (if diference in acitivity levels is >25%, then thiamine deficiency)" "Describe the general structure, regulation, and required cofactors/vitamins of the PDC complex
- CORRECT ANSWER glucose and pyruvate cycle to the PDC, which produces acetyl CoA -->
CO2 and lipids (which cycle back) high blood glucose activates = high pyruvate, high NAD+, high ADP low blood glucose inhibits = high ATP, high NADH, high acetyl-CoA (end product inhibition) PDC is inactive during gluconeogenesis, active during glycolysis -Ca2+ is a strong activator of phospatase, and thus PDC"
"Describe the cellular location and reactions of the citric acid cycle that lead to the production of
reducing equivalents that are oxidized in the electron transport chain to yield ATP - CORRECT
ANSWER Can Intelligent Karen Solve Some Foreign Mafia Operations //
Citrate - Isocitrate - Ketoglutarate - Succinyl-CoA - Succinate - Fumarate - Malate - Oxaolacetate yields 10 ATP per cycle per Ac-CoA, 8 electrons occurs in mitochondria" "Describe the effect of the following parameters on the activity of the TCA cycle and the
mechanisms by which the effect occurs: mitochondrial NAD+/NADH ratio, ADP/ATP ratio -
CORRECT ANSWER high NAD+/NADH ration speeds up cycle
-inhibited by NADH high ADP/ATP ratio speeds up cycle -activated by ADP" "Describe the central role of the TCA cycle in connecting glycolysis, gluconeogenesis, oxidative
phosphorylation, fatty acid metabolism, and amino acid metabolism - CORRECT ANSWER
electrons from glucose oxidation feed into ETC, driving ATP synthesis" "Describe the main cataplerotic and anaplerotic pathways that permit the efflux and
replenishment of citric acid cycle intermediates. - CORRECT ANSWER cataplerotic pathways =
efflux for use in other metabolic pathways, in liver -high glucose, ATP unused, NADH high --> inhibits isocitrate dehydrogenase and a-ketoglutarate dehydrogenase -excess citrate shuttled to cytoplasm and used for FA synthesis / a-ketoglutarate is used for AA synthesis anaplerotic pathways = refills intermediates of TCA cycle -as amount of OAA is depleted, citrate synthase reaction decreases and causes acetyl CoA concentration to increase, activating Pyruvate carboxylase to produce more OAA
- pyruvate carboxylase (biotin)"
