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MCM > Mitochondria Bioenergetics > Flashcards

Mitochondria Bioenergetics Flashcards

1
Q

In glycolysis, we made 2 ATP, 2 NADH and 2 pyruvate. What must be do next?

A

We need to remake NAD+.

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2
Q

Before we begin the TCA cycle, what do we want to do?

A

Convert 3 carbon pyruvate to 2 carbon acetyl group part of acetyl coA.

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3
Q

When we converted pyruvate to a 2 carbon acetyl group part of acetyl coA, what happened to the carbon?

A

Pyruvate was decarboxylized by the PDC and it was lost as CO2

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4
Q

What is responsible for a majority of carb, protein and fat oxidation?

A

The TCA cycle

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5
Q

What are we doing in the TCA cycle?

A

oxidizing carbon so that we can harness the NRG.

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6
Q

Is the TCA cycle anabolic, catabolic or amphibolic?

A

Amphibolic

Both catabolism and anabolism will occur. Remember, its a cycle.
We have to build up and build down.

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7
Q

Where does the TCA cycle occur?

A

Mitochondrial matrix

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8
Q

3 stages of TCA cycle

A
  1. Break down carbs, fats and proteins
  2. Convert the breakdown products into acetyl co-A
  3. Allow acetyl co-A to enter the TCA cycle
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9
Q

Products of the TCA cycle are

A

3 NADHs,
1 FADH2
1 GTP

And 2 CO2s are released.

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10
Q

Why is the TCA cycle important?

A

it is the driver of cellular respiration. It takes acetyl coA and harvest energy in the form of NADH, FADH2 and ATP. The reduced electron carriers are then taken to the ETC and though oxidative phosphorylation, generate most of the ATP we use!

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11
Q

Acetyl co-A is a activated form of _______ and can be made from three sources:

what sources and how

A

acetate.
Acetyl coA can be made from

  1. Carbs
    Glucose–> pyruvate via oxidation
    Pyruvate–> Acetyl CoA via decarboxylation
  2. Fats
    TAGS–> FA–> acetyl CoA via B oxidation
  3. Proteins
    AA are converted to acetyl CoA
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12
Q

In acetyl coA, where is the high NRG bond?

A

thioester bond

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13
Q

Pyruvate is made in the cytosol but the TCA cycle occurs in the mitochondrial matrix.
how does pyruvate enter the mitochondria?

A

Pyruvate will enter the MT matrix using a MPC (mitochondrial pyruvate carrier)

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14
Q

How do we convert pyruvate to acetyl coA?

A

Pyruvate is converted to acetyl CoA through the PDC.
The PDC will decarboxylize pyruvate in a series of reactions to create acetyl coA.

2 NADHs are made and a CO2 is released

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15
Q

When is the PDC inactive?

A

PDC is inactive when it is phosphorylated.

Thus, the PDC is always phosphorylated to make sure that it is not always on and we are not always going through the TCA cycle.

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16
Q

How do we ensure that we are not always going through the Krebs cycle?

A

the PDC is always phosphorylated, making it INACTIVE.

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17
Q

So the PDC is active when it is

A

dephosphorylated

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18
Q

What happens when we have a shit ton of pyruvate, but our body is deficient in phosphotases?

A

If we are deficient in phosphotases, our PDC cannot be dephosphorylated, which means it cannot be turned on.

Pyruvte must utilize another method: lactic acid will be made INSTEAD of acetyl coA

Thus, people who have a buildup of pyruvate but lack phosphotases will often get LACTIC ACID BUILDUP!

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19
Q

What should people who have a lot of pyruvate, but little phosphotases becareful of?

A

They should avoid to further build up of pyruvate. thus, they should avoid ALANINE because alanine is converted to pyruvate.

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20
Q

In a high NRG state, do we want to keep the pyruvate system going fast?

A

No. It should run smoothly. So, if we are in a high NRG state we want it to slow down.

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21
Q

Inhibitors of PDC

A

NADH
ATP
Acetyl CoA

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22
Q

Activators of PDC

A

Pyruvate and

ADP

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23
Q

If we are in a low energy state, what do we do with the TCA cycle?

A

We need NRG we so want to upregulate it.

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24
Q

aerobic respiration is coupled with ______

A

OxPhos

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25
Q

__ steps in the TCA cycle

A

8

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26
Q

1st step in the TCA cycle

A

[OAA+ acetyl coA]–> citrate via citrate synthase

Co-A is kicked off.

This is a irreversible regulatory step.

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27
Q

2nd step

A

citrate–>isocitrate

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28
Q

3rd step

A

[isocitrate–> alpha keto glutarate] via isocitrate DH.

Isocitrate DH is the rate limiting step.
NAD+ is reduced to NADH
CO2 is lost

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29
Q

4th step

A

[alpha ketoglutarate–> succinyl coA] via alpha keta glutrate DH

REgulated step

NAD+ is reduced to NADH
CO2 is lost

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30
Q

5th step

A

[succinyl co-A]–> succinate

via succinate thiokinase
GTP is made

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31
Q

6th step

A

[Succinate–> fumarate]

Succinate DH

FADH2 is made

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32
Q

7th step

A

fumarate–> malate

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33
Q

8th

A

Malate–> OAA via malate DH

3rd and final NADPH is a made

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34
Q

What are the 3 regulated, irreversible steps?

A
  1. Citrate synthase
  2. Isocitrate DH
  3. Alpha keto glutarate DH
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35
Q

Where is NADH made?

A

3 NADHs are made.

1. isocitrate DH
CO2 is also lost
2. alphaketo glutarate DH
CO2 is also lost
3. Malate DH
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36
Q

What is the rate limiting step?

A

Isocitrate DH,

when isocitrate–> alpha ketoglutarate.

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37
Q

Where is our GTP made

A

GTP is made by succinyl thiokinase

succinyl co-A–> succinate

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38
Q

Where is FADH2 made?

A

Succinate–> fumarate

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39
Q

When ATP levels are low, the TCA cycle is ______

A

increased

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40
Q

Do we continue with the TCA cycle when we have high levels of ATP?

A

No. TCA and ETC are inhibited

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41
Q

Anapleurtic

A

Anapleuritic reactions are those that allow intermediates to enter the TCA cycle

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42
Q

does the TCA cycle allow anapleuritic reactions?

A

YES! Intermediates can enter the TCA cycle at various points

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43
Q

When we are in a low NRG state, what activates the PDC complex?

A

high Ca2+ will activate the PDC complex when we are low in NRG

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44
Q

Entry sites for AA

A 
There are 4 entry sites for AA:
OAA,
Alpha ketoglurate
Succinyl CoA
Fumurate
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45
Q

What enters alpha keto glutarate

A
  1. Gln
  2. Arg
  3. Pro
    4 His

will be converted to glutamate and enter alphaketo

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46
Q

What enters succinyl CoA?

A

Threonine
Isoleucine
Methionine
Valine

converted to propionyl CoA

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47
Q

What enters at fumarate?

A

Phe
Asp
Tyr

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48
Q

What enters at OAA

A

Asp

Asn

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49
Q

TCA cycle can also provide intermediates for pathways

A
  1. FA synthesis—> citrate

2. gluconeogensis–> malate

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50
Q

Succinyl coA can be used to maek ______, which we useto make ______

A

Succinyl coA can be used to make PORPHYRIN, which we use to make HEME

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51
Q

Disorders of the TCA cycle are common?

A

No. they’re rare and your brain is the first to be affected

52
Q

2 disorders of the TCA cycle

A

2 oxoglutaric aciduria

Fumurase deficiency

53
Q

How can we test for both?

A

urinalaysis

54
Q

in 2 oxiglutataric acid and fumarase deficency, what is the first neuro system to be affected

A

neural

55
Q

2 oxoglutaric aciduria

Fumurase deficiency are autosomal

A

recessive

56
Q

2 oxoglutaric acis sx

A
  1. metabolic acidosis because we are excreting 2 oxoglutaric acid
  2. encephalopathy
  3. mental retardation
57
Q

how can we check for 2 oxoglutaric aciduria

A

we can look at a UA for metabolic acidosis and in crease in 2 oxoglutarate

58
Q

Presentation of fumarse deficiency

A
  1. death before <10

2. encephalopathy with speech delays without metabolic acidosis

59
Q

detect for fumarase deficiency

A

Increased excretion of fumurase, followed by excretion of succinate and lactate and followed by 2 oxoglutarate

60
Q

Is excretion found all of the time in patients with fumurase?

A

almost, but it is not always fumurase

61
Q

Is there any tx for these dx?

A

no

62
Q

How are these two dx similar

A

can cause

  1. hypotonia
  2. spasticity
  3. developmental delays

both can cause acute metabolic acidosis and lead to hypoglycemia

most are leth <10

63
Q

fumarase deficiency; we can see excretion of

A

fumurate, succinate, alpha keto glurate and citrate

64
Q

SCS

A

Succicyl CoA Synthestase deficiency is thought to be caused by mutations in the SUCLA2 and SUCLG1 subunits.

As a result, we are going to have problems metabolizing succinate and we will have low mT content

65
Q

As a result of SCS, we will have

A

problems metabolizing succinate and low mT dna content

66
Q

Sx of SCS

A
  1. Methylmalonyl aciduria
  2. hypotonia
  3. distonia
  4. muscular atrophy
  5. sensory and neural impairment
67
Q

Where does oxphos take place?

A

intermembrane space of the MT

68
Q

What occurs in the MT matrix?

A
  1. TCA cycle

2. FA oxidation

69
Q

The pH is higher/lower in the mT matrix

A

HIGHER

70
Q

Can things enter the mT?

A

YES! the mT has porins that are located on the outside membrane , aloowing things to enter.

71
Q

There are 2 types of redox reactions

A
  1. electron only transfer

2. reducing equivalent transfer

72
Q

Electron only transfer

A

electrons are transferred between 2 metal ions

73
Q

_____ are always on the side the the electrons

A

oxidants

74
Q

Reducing equivlanet transfer

A

there is a transfer of a H and a electrons

75
Q

What is E0

A

the standard redox potential

76
Q

Reducing agent is being ______

A

oxidized

77
Q

Oxidizing agent is being ______

A

reduced

78
Q

Smaller E0

A

means that the substance has LESS affinity for the electrons and wants to give them up

79
Q

Higher E0

A

substance has MORE affinity for the electrons and wants them

80
Q

Which will have the smaller E0: reducing agent or oxidiizing agent?

A

Reducing agent

81
Q

Which will have the higher E0: reducing or oxidizing agent?

A

Oxiding agent because its getting reduced (RIG)

82
Q

how will electrons transfer in a redox pair?

A

from low E0 to high E0

83
Q

Difference in E0

A

delta G

84
Q

How are E0 and standard free NRG related

A

inversely realted

85
Q

OxPhos occurs where?

A

inner mT membrane

86
Q

A successful oxphos must

A
  1. transfer the electrons from NADH and FADH2 to O2
  2. Create proton gradient
  3. which will make ATP
87
Q

Electrons are transferred through a _________ and use the NRG to do what?

A

Electrons are transferred through a RESPIRATORY chain and use the NRG to pump H+ from the mT matrix, into the inner membrane space

88
Q

what is the proton motive force

A

the force that promotes H+ ions to be pumped across the membrane

89
Q

What creates the PMF

A
  1. pH gradient

2. membrane potential

90
Q

pH gradient

A

As H+ are being pumped across the membrane, the inner membrane space will become more acidic

91
Q

membrane potential

A

as protons are being pumped from mT membrane–> inner membrane space, the inside will become more -

92
Q

The creation of ATP is made by

A

ATP synthase (complex v)

93
Q

How many H+ are required

A

3+1

3 H+ must pass through the channel and 1 must be used for the translocation of ADP

94
Q

What disrupts proton transport through ATPase synthase

A

Oligomycin

95
Q

OxPhos is mediated by what?

A

Respiratory chain

96
Q

What is the respiratory chain?

A

The respiratory chain is a complex of proteins that allows the transfer of electrons:

Complex I-V
Cytochrome C
CoQ (ubiquinone)

97
Q

Mobile carriers in respiratory chain

A

Cytochrome C and CoQ (ubiqionone)

98
Q

What is CoQ

A

a lipophillic molecule that is a mobile carrier.

99
Q

___ receives NADH

A

C1

100
Q

___ receives FADH2

A

C2

101
Q

What complex converts 1/2 oxygen to water?

A

CIV

102
Q

How are electrons transferred

A

NADH enters are complex 1
FADH2 enters at complex 2

both go to CoQ–> C3–> cyctochrome C–> C4, where the electrons go to O to convert to water.

103
Q

What tells us the intactness of the mT

A

cytochrome C/

104
Q

is CoQ a prosthetic group for C3?

A

no. its a lipophillic molecule.

105
Q

Which complexes are pumping protons into the inner membrane space?

A

I, III and IV

106
Q

Oxphos is sensentive to

A

O2 and

[ATP/ADP] ratios

107
Q

Summary of ETC

A

NADH and FADH2 donate their electrons to the ETC. Electrons are being transported, creating NRG.

This NRG is used to pump protons (I, III and IV) into the inner membrane space. AS a result, a proton gradient and ion gradient are being created. These two gradients create NRG and are used to power ATP synthase, allowing the creating of ATP. H+ is pumped back into the mT membrane

108
Q

Uncoupling says that

A

electron transfer is COUPLED to proton gradient

109
Q

If the proton gradient is disrupted, what happens to ADP?

A

ADP uncouples from P and cannot be phosphorylated

110
Q

Result of uncoupling

A

heat will be created (no ATP synthesis) by permitting proton influx (via UCPs) WITHOUT creating ATP.
Thus, they disrupt the proton gradient and do not allow ADP to couple with Pi.

111
Q

In uncoupling, what happens to the TCA cycle and electron transfer to O2?

A

They receive signals that there is no ATP and TCA and electron transport CONTINUE! allowing bears to live in the summer :)

112
Q

How can we pump H+ ions into the matrix in uncoupling?

A

Uncoupling proteins like thermogenin (UCP-1), aspirin and DNT are inserted into the membrane and allow the transfer.

113
Q

What do uncoupling protein do?

A

They will allow heat to be created by permitting proton influx WITHOUT creating ATP.
Thus, they disrupt the proton gradient and do not allow ADP to couple with Pi.

114
Q

Heat generates

A

brown fat tissue

115
Q

in hibernating animals, they do not eat, so they dont make ATP. How do they maintain body temperature?

A

a UCP (thermogenin) is expressed. This will allow the ATPase to still spin and generate heat

116
Q

How do high NRG substances like FADH2 and NADH enter the MT?

A

Shuttle systems. Reduced NADH cannot enter the membrane

117
Q

Oxphos occurs where?

A

inner mT membrane

118
Q

Malate-aspartate shuttle system transports what?

A

NADH from the [cytosol into the mT matrix]

119
Q

Glycerolphosphate system transports

A

transports FADH2 from [cytsol–> inner mT membrane].

120
Q

How does the malate-aspartate system work?

A

NADH cannot pass the membrane.
So, its electrons are given to malate.
Malate is shuttle via malate-aspartate shuttle.
Malate will then go and transfer electrons to NAD in the matrix to be used in the TCA cycle

121
Q

Glycerolphosphate shuttle mechanism

A

Pyruvate transfers electrons to glycerol 3 phosphate.

Glycerol3phosphate is then transferred into the mT via the glycerolphosphate system.

electrons from G3P are then donated to FAD

122
Q

Malate aspartate shuttle operates in the

A

heart
liver
kidneys

123
Q

In a well-fed stat, what reaction is responsible for transport of NADH from cytsol–> MT?

A

malate aspartate shyttle

124
Q

glycerolphosphate shuttle works where?

A

brain and muccle

125
Q

FADH2 from glycerolphosphate system will join the ETC at ___

A

CoQ

MCM (12 decks)

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