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MSAP Week 2 > Week 2 Biochem > Flashcards

Week 2 Biochem Flashcards

1
Q

The Pentose phosphate pathway creates ______ to use for ________ in anabolism.

A
  1. NADPH

2. Reducing Power

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2
Q

After becoming G-6-P in the cells, glucose undergoes ________ to yield ______. In anaerobic cells, this is then converted into ______. In aerobic cells, it then enters the _______, is utilized in ________, and yields ______.

A
  1. Glycolysis
  2. TWO Pyruvate
  3. Lactate
  4. Mitochondria
  5. The electron transport chain
  6. ATP
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3
Q

The GLUT-2 transporter is found in _______, and is characterized as _______.

A
  1. The Liver

2. Insulin-Independent

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4
Q

The GLUT-4 transporter is found in _______, and is characterized as _______.

A
  1. Skeletal muscle and adipose tissue

2. Insulin-Dependent

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5
Q

_______ is the only metabolic process that is able to produce ATP anaerobically. It is also said to be ________, because regulation of it may be different between species/life forms.

A
  1. Glycolysis

2. Ubiquitous

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6
Q

Glucose is structurally considered an ___________, meaning that it has: _______

A
  1. Aldo-hexose

2. An aldehyde on the end of its 6-carbon chain

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7
Q

Pyruvate is structurally considered an _______.

A

Alpha keto acid

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8
Q

Glycolysis inputs: (which is oxidizer/reducer)

Glycolysis outputs:

A
  1. Inputs:
    • 2 ATP = oxidizer
    • 2 NAD+ = reducer
  2. Outputs:
    • 2 NADH (reduced)
    • 4 ATP (oxidized)
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9
Q

Glycolysis is broken into 2 Stages:
The first stage involves ________ and is referred to as the ________. The second stage involves ______ and is referred to as the _________.

A
  1. Input of 2 ATP
  2. Priming stage
  3. Oxidation of ATP to yield a net of 2 ATP
  4. Payoff Stage
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10
Q

Describe how one might also split glycolysis into 3 phases:

A

Stage 1: Activation= 2 ATP consumed
Stage 2: Isomerization= Splitting of hexose-bisphos.
Stage 3: Oxidation: Of Glyceral-3-P to form ATP/NADH

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11
Q

What are the 3 types of rxns involved in glycolysis?

A
  1. Breakdown of carbon skeleton
  2. Phos. of ADP
  3. Formation of reduced coenzyme - NADH
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12
Q

The first step of glycolysis consumes a molecule of ATP and is therefore considered to be _______.

A

Exergonic

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13
Q

What is the most important regulatory enzyme of glycolysis? Why? Also, What type of enzyme is this?

A
  1. Phosphofructokinase-1 (PFK-1)
  2. After it conducts its catalytic activity, the molecule MUST continue through glycolysis to yield pyruvate.
  3. Allosteric Enzyme
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14
Q

The glycolytic pathway is OVERALL considered to be ______.

A

Exergonic

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15
Q

Why is the 4th step of glycolysis driven toward a net breakdown of G-6-P?

A

Because the products of that reaction are taken away, creating a need for more to be made.

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16
Q

ALL reactions of the glycolytic pathway occur in _______.

A

The Cytoplasm

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17
Q

What are the 4 major fates of Pyruvate after being formed from glycolysis?

A
  1. Acetyl CoA: For mitochondrial ATP production
  2. Ethanol: In yeasts/bacteria to produce NAD+ and continue glycolysis anaerobically
  3. Lactate: Same as ethanol, but in eukaryotes
  4. Oxaloacetate: 1st step of gluconeogenesis
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18
Q

Why must the cell maintain separate pools of NAD+/NADH?

A

The NADH molecule signals that the cell is in a high energy state and is therefore regulatory in nature. Since reactions are occurring separately in the cytoplasm and mitochondria, they must each have their own pool as a regulator.

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19
Q

Which enzyme catalyzes the conversion of pyruvate to L-Lactate in anaerobic metabolism

A

Lactate Dehydrogenase

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20
Q

When does the reverse reaction (L-Lactate becomes Pyruvate) occur?

A

Under Aerobic Conditions

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21
Q

Red blood cells have no ______, and therefore they can only use ______ to generate ______. This means they are constantly undergoing ______.

A
  1. Mitochondria
  2. The Glycolytic Pathway
  3. ATP
  4. Lactic Acid Fermentation (Lactate–>Pyruvate)
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22
Q

What is the main point of alcoholic fermentation of pyruvate to ethanol in yeasts?

A

To produce NAD+ for the glycolytic pathway to continue

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23
Q

In the presence of oxygen, newly formed pyruvate will then ________ in order to ______.

A
  1. Enter the mitochondria

2. Complete Oxidation

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24
Q

In order to enter the mitochondria, pyruvate must be ______ to form the ______.

A
  1. De-carboxylated (by Pyr. De-H-ase)

2. Pyruvate Dehydrogenase Complex

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25
Q

Pyruvate entering the mitochondria will ultimately form _____ which will go on to be used in ______.

A
  1. Acetyl CoA

2. The T.C.A. cycle

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26
Q

What is the function of Insulin?

A

To move GLUT-4 transporters from the cytoplasm (basal state) to the cell surface to allow uptake of glucose in response to glucose intake

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27
Q

Why is Glucokinase not regulated? How IS Hexokinase regulated?

A
  1. Because in the liver, Glucose uptake is constantly possible due to GLUT-2 transporters
  2. By Glucose-6-Phosphate formation. A buildup will signal these cells that Glycolysis can be inhibited (feedback inhibition).
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28
Q

How is PFK-1 DOWN regulated? (2)

A
  1. An abundance of ATP will signal that the cell is in a high energy state and exhibit feedback inhibition on PFK-1
  2. An abundance of Citrate from the C.A.C.
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29
Q

How is PFK-1 UP regulated? (2)

A
  1. Abundant AMP signals a low energy state.

2. Fructose-2,6-Bisphosphate affects substrate affinity

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30
Q

Insulin from Beta Cells ________ glycolysis.
Glucagon from Alpha Cells ______ glycolysis.
Both are able to determine levels of ______ in the ______.

A
  1. Stimulates
  2. Decreases
  3. Fructose-2,6-Bisphosphate
  4. Liver
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31
Q

The insulin receptor activates a ________ and almost always ultimately regulates metabolic pathways by activating _______.

A
  1. Receptor Tyrosine Kinase

2. Phosphatases

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32
Q

What is the function of PFK-2? What enzyme reverses this action?

A
  1. To convert Fructose-6-Phosphate into Fructose-2,6-Bisphosphate.
  2. Fructose-2,6-Bisphosphatase
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33
Q

What effect does Insulin have by activating phosphatases in liver cells?

A

Those phosphatases DEphosphorylate PFK-2 in order to INCREASE its sugar KINASE activity of converting Fructose-1,6-BP into Fructose-2,6-BP, but also DECREASE its sugar PHOSPHATASE activity.
*Ultimately= INCREASE Fructose-2,6-BP to be converted into Fructose-1,6-BP

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34
Q

What enzyme converts Fructose-2,6-BP into Fructose 1,6-BP? Under what conditions does this reaction occur?

A
  1. PFK-1
  2. High blood sugar: Since the liver is freely taking up glucose, this is when Insulin can signal the liver to speed up glycolysis (due to an abundance of glucose).
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35
Q

What happens when Glucagon binds its glucagon receptor?

A

The GPCR pathway activates PKA, which phosphorylates PFK-2. This INHIBITS its sugar kinase and ACTIVATES its sugar phosphatase, REDUCING the amount of Fructose-2,6-BP in the liver cells, and slowing glycolysis.

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36
Q

Why does an increase in Fructose-2,6-BP speed up glycolysis?

A

It INCREASES the affinity of PFK-1 for its substrate, Fructose-6-Phosphate (lowers its Km).

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37
Q

Pyruvate Kinase is inhibited by ____ and ____. It is activated by _____ and ______.

A
  1. ATP (high energy intermediate)
  2. Acetyl CoA (fuel from FA oxidation)
  3. AMP abundance (low energy intermediate)
  4. Fructose-1,6-BP (feed-forward mechanism because it has been committed)
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38
Q

How does Glucagon in the LIVER regulate Pyruvate Kinase activity?

A

The end result of Glucagon binding its receptor in the liver is activation of a KINASE, which phosphorylates Pyruvate Kinase to deactivate it and inhibit glycolysis.

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39
Q

In the Liver, Fructose can enter Glycolysis at the ______ stage.

A

3-Carbon (as DHAP and G-3-P)

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40
Q

Fructose is structurally considered a _______.

A

Keto-Hexose

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41
Q

What is the first step of Fructose metabolism (in the liver) for use in glycolysis?

A

Fructokinase converts it into F-1-P

42
Q

What is the second step in Fructose metabolism (in the liver) for use in glycolysis?

A

Aldolase B converts F-1-P into DHAP and glyceraldehyde

43
Q

Why is deficiency of Fructokinase considered benign but deficiency of Aldolase B is potential lethal?

A

Because Fructose can be readily metabolized and excreted in the urine, whereas a build up of F-1-P will lead to liver problems since there will be a loss of hepatic phosphate (decreased hepatic ATP) since the phosphate is tied up in F-1-P.

44
Q

What is the 1st step in Fructose metabolism in the muscle for use in glycolysis?

A

Phosphorylation by Hexokinase, converting it into F-6-P which enters directly into glycolysis

45
Q

If a person has Aldolase B deficiency, what dietary restrictions must they implore and why? If a person has a deficiency in ANY of the 3 Galactose metabolizing enzymes, what dietary restrictions must they implore and why?

A
  1. Fructose avoidance (i.e. Sucrose, Fructose, honey, etc.) because the buildup of F-1-P will occupy all liver phosphate.
  2. Lactose avoidance because it can form galactose and cause buildup in the liver.
46
Q

What are the 3 counter-regulatory hormones of Insulin?

A
  1. Glucagon
  2. Epinephrine
  3. Cortisol
47
Q

In the absence of cAMP, PKA exists as _______. This form consists of _________.

A
  1. An inactive tetramer

2. TWO regulatory and TWO catalytic subunits

48
Q

What specifically does binding of cAMP to PKA cause?

A

Dissociation of the catalytic subunits that act as protein kinases

49
Q

List the 3 common catabolic pathways:

A
  1. TCA Cycle
  2. Electron Transport Chain
  3. ATP synthesis (Cellular Respiration)
50
Q

What is the link between glycolysis and the TCA cycle for the complete oxidation of glucose?

A

The Pyruvate Dehydrogenase Complex

51
Q

What are the 3 soluble substrates for the PDH complex?

A
  1. Pyruvate
  2. Coenzyme A
  3. NAD+ (electron acceptor)
52
Q

What are the 3 enzyme-bound CoFactors of the PDH complex?

A
  1. Thiamine-Pyrophosphate (Vitamin B1)
  2. Lipoic Acid
  3. FAD+/FADH2 (electron acceptor)
53
Q

What makes the PDH so efficient?

A

Each reaction is coupled to the next through channels within the enormous enzyme complex

54
Q

At the end of one cycle of AcetylCoA formation (by the Pyruvate Dehydrogenase complex), what are we left with and how does it re-enter the cycle?

A
  1. NADH

2. It enters the electron transport chain to be converted back into NAD+.

55
Q

What kind of feedback inhibition does the PDH complex exhibit?

A
  1. Buildup of NADH and AcetylCoA inhibit the PDH complex from making more of them.
  2. Buildup at ATP will inhibit allosterically , while ADP buildup will stimulate allosterically.
56
Q

How do kinases and phosphatases play a role in regulation of the PDH complex?

A
  1. Phosphorylation by PDH complex kinase will DECREASE activity of it.
  2. Dephosphorylation by the PDH complex phosphatase will INCREASE activity of it.
57
Q

What factors increase the PDH activity? (2)

A

Insulin and Ca2+

58
Q

What enzyme converts pyruvate into oxaloacetate?

A

Pyruvate carboxylase

59
Q

What does “TCA Cycle” stand for?

A

Tricarboxylic Acid Cycle

60
Q

What does the TCA cycle facilitate?

A

Complete oxidation of AcetylCoA to CO2

61
Q

Name the Tricarboxylic Acid referred to in the TCA Cycle:

A

Citrate (Citric Acid)

62
Q

Where does the TCA cycle occur?

A

In the Mitochondrial Matrix

63
Q

In the TCA cycle, electron are accepted by _______ to form the reduced coenzymes _______.

A
  1. NAD+ and FAD

2. NADH and FADH2

64
Q

How is the TCA cycle amphibolic?

A

Its ultimate goal is to form energy molecules, NADH and FADH2, but many of its intermediates, like Citrate, can be used to form fatty acids and steroids for example.

65
Q

How is the TCA cycle anaplerotic?

A

May intermediates of the cycle can be put back into the cycle to continue along in it and produce energy.

66
Q

What happens to the oxaloacetate used in the 1st step of the TCA cycle? Why is this important?

A

It is eventually reformed during the cycle. This shows that there is no net change in the amount of inputs used in the cycle.

67
Q

Which is the only enzyme involved in the TCA that is actually embedded in the mitochondrial membrane?

A

The Succinate Dehydrogenase Complex

68
Q

Activators and Inhibitors of Citrate Synthase:

A 
Activators:
  -Ca2+
  -ADP
Inhibitors:
  -ATP
  -NADH
  -Succinyl-CoA (feedback from committed steps)
69
Q

Why is calcium an activator of several metabolic enzymes in the TCA cycle and other pathways?

A

It is a signal from muscle cells that there is a high energy demand due to muscle contraction.

70
Q

Activators and Inhibitors of Isocitrate De-H-ase:

A 
Activators:
  -Ca2+
  -ADP
  -NAD+
Inhibitors:
  -ATP
  -NADH
71
Q

Activators and Inhibitors of Alpha-Ketogluturate De-H-ase complex:

A 
Activators:
  -Ca2+
  -AMP
Inhibitors:
  -ATP
  -GTP
  -NADH
  -Succinyl CoA
72
Q

What is the most important regulator of the TCA Cycle and why?

A
  1. AMP
  2. Because it’s change in concentration from a rest to exercise state exhibits an almost 1000 fold increase, which is much more obvious than the same relative change in ADP or ATP.
73
Q

Define Anapleresis:

A

“Filling Up”, which implies that reactants in these reactions exhibit no net change in amount in any one cycle, and have a duel nature to create energy molecules as well as materials for biosynthesis of other biomolecules.
i.e. The intermediates are replenished

74
Q

What are 3 other ways that intermediates can enter the TCA Cycle?

A
  1. Pyruvate —> Oxaloacetate
  2. Aspartate —> Oxaloacetate
  3. Glutamate —> Alpha-KG
75
Q

Define Transamination:

A

Transferring an Amine group from an Amino Acid to an alpha-keto acid to form a NEW Amino Acid and a NEW alpha-keto acid.

76
Q

Describe the reaction that Aspartate undergoes to enter the TCA cycle: (Give the type of Reaction and Enzyme responsible as well)

A
  1. Transamination
  2. Aspartate Transaminase (and Vitamin B6)
  3. Aspartate in abundance donates an amino group to alpha-KG to form Glutamate, while accepting Aspartate itself becomes Oxaloacetate.
77
Q

Describe the reaction that Glutamate undergoes to enter the TCA cycle: (Give the Enzyme responsible as well)

A
  1. Glutamate De-H-ase

2. Glutamate gets rid of ammonia (NH3) to become alpha-KG, but can also work in reverse.

78
Q

The ETC essentially functions to move electrons directly into ________ in order to power ________. This creates ________ which is used for ______.

A
  1. The mitochondrial inner membrane
  2. The pumping of protons into the inter-membrane space
  3. A pH gradient
  4. The formation of ATP
79
Q

Define Cristae:

A

Highly convoluted folds of the inner mitochondrial membrane

80
Q

While the outer mitochondrial membrane is ______ (and contains lots of ______ to give it rigidity, the inner membrane is actually ______ does not contain this substance.

A
  1. Not very selective (highly permeable)
  2. Cholesterol
  3. VERY selective
81
Q

What is meant by Oxidative Phosphorylation?

A

ADP + Pi —> ATP

82
Q

List the 5 components of the ETC:

A
  1. Flavoproteins
  2. Copper-Containing Proteins
  3. Iron-Sulfur Proteins
  4. Ubiquinone
  5. Cytochromes
83
Q

Flavin structure has ______, making it very ______. This is important because ______.

A
  1. THREE Rings
  2. HYDROPHOBIC
  3. When it transfers electrons it releases them AS hydrogen atoms.
84
Q

Ubiquinone possesses a ___________, making it very _______.

A
  1. 30-50 Carbon tail

2. Hydrophobic

85
Q

Cytochrome molecules contain __________, which consists of _______. They are involved in ______.

A
  1. A heme group
  2. A porphyrin ring and an Iron atom
  3. 1 electron transfer
86
Q

How do Iron-Sulfur proteins differ from Cytochromes? How are they similar?

A
  1. (Differ) Their Iron atom is attached to Cysteine or FREE sulfur inside of a protein, but NOT heme.
  2. (Similar) They are both involved in 1 electron transfer.
87
Q

Copper-bound ions are involved in ______.

A

1-electron transfer

88
Q

Which is the only 1 of the 5 components involved in ETC complexes that is associated with MORE than 1 electron transfer?

A

Flavoproteins (Flavin)

89
Q

Of the 5 ETC complexes, which are involved in electron transfer? What is the goal of the other complexes?

A
  1. Complexes 1-4 are involved with electron transfer

2. Complex 5 is the ATP synthase that functions in assembly of ATP

90
Q

Ubiquinone is also called ______.

A

Coenzyme Q

91
Q

What is the chemiosmotic hypothesis?

A

ATP synthase is driven by the electrochemical gradient created by the pumping of protons from the mitochondrial matrix to the inter-membrane space.

92
Q

The electrochemical gradient favors ________.

A

The movement of H+ back into the mitochondrial matrix

93
Q

Protons pass through a ________ located in _______. ATP synthase then catalyzes _______.

A
  1. H+ channel (back into the matrix)
  2. The base of ATP synthase
  3. The phosphorylation of ADP
94
Q

Describe the 2 components of ATP synthase:

A
  1. F-0:
    • Integral to the membrane
    • Hydrophobic
    • IS the transmembrane channel for H+ movement
  2. F-1:
    • Catalyzes ATP synthesis
    • Coupled to rotation unit (gamma subunit)
    • TURNS as protons pass through F-0
95
Q

How SPECIFICALLY is the proton gradient harnessed for ATP synthesis?

A

The passing of H+ through the F-0 channel POWERS the rotation of the gamma subunit that moves the catalytic F-1 subunit

96
Q

How does ADP get back into the mitochondrial matrix? (And vice versa, how does ATP leave the matrix?)

A

The ADP/ATP Translocase exchanges them through both membranes and is powered BY the same proton gradient.

97
Q

What is Atractyloside?

A

A plant toxin that can inhibit the ADP/ATP Translocase by blocking ADP entry into the matrix

98
Q

What is the difference between primary and secondary active transport?

A

Primary: Relies on ATP hydrolysis to power activity
Secondary: Relies on concentration gradient of some other source for power

99
Q

What is the MAIN control of ATP synthesis?

A

The availability of ADP in the matrix controls oxygen consumption for ATP synthesis

100
Q

How many ATP equivalents can be produced from 1 molecule of:

  • NADH: ____
  • FADH2: ____
A
  1. NADH = 2.5

2. FADH2 = 1.5

101
Q

What 3 processes must be considered in tallying the total number of ATP molecules that can be produced from ONE substrate level phosphorylation and the oxidation of NADH and FADH2?

A
  1. Glycolysis
  2. PDH Complex
  3. TCA Cycle
102
Q

Why do early models of maximal ATP production per substrate level phosphorylation exhibit OVER-estimation of total ATP production?

A

Because they don’t take into account that we lose some of the proton gradient due to the Phosphate-Hydrogen symporter and also to the ADP/ATP-Translocase.

MSAP Week 2 (3 decks)

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