Catabolism and bioenergetics: how do we make ATP Flashcards

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1
Q

What is the energy metabolism?

A

The process of using carbon and oxygen to make chemical energy in the form of ATP.

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2
Q

What happens in the catabolic pathways?

A

Carbon sources are broken down.

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3
Q

What do we need to do to have energy in our life?

A

Turn energy in a usable form.

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4
Q

Where is the current energy in our body?

A

In the cell.

In a molecule called adenosine triphosphate or ATP.

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5
Q

Where is chemical energy?

A

Locked in its phosphodiester bonds.

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6
Q

What happens when the phosphodiester bonds break down?

A

The energy released can be used to drive reactions.

Biosynthesis, mechanical work, transport.

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7
Q

Why is ATP important?

A

It allows reactions to occur that otherwise would be impossible.
Provides a link between energy consuming and energy producing reactions.

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8
Q

How much ATP does our heart need?

A

6kg/day.
700 mg/one time.
Efficient at making it and not stop for breath.

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9
Q

What do we need to do first to turn energy into a usable form of ATP?

A

Break down a carbon source, lipid, polysaccharide, protein into its parts.
Feed its parts in the energy producing pathways.

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10
Q

What do we break down in humans?

A

Starch and sugars from food.

Or glycogen stored in liver –> ribose + hexose sugars –> hydrolysed into 3 carbon sugars –> converted into pyruvate.

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11
Q

Where does the break down of starch and sugars occur in humans?

A

In the cytoplasm.

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12
Q

How does the break down of starch and sugars in humans called?

A

Glycolysis = sugar breakdown.

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13
Q

What is the result of the conversion of 3 carbon sugars into pyruvate?

A

The release of 1 molecule of ATP.

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14
Q

How many ATP molecules does hexose sugar, like glucose produce?

A

2 ATPs.

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15
Q

What do we need in order to generate ATP efficiently and avoid generating the by product lactate?

A

Mitochondria for oxidative phosphorylation.

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16
Q

How many ATP molecules can be produced by the oxidative phosphorylation where mitochondria are involved?

A

38 ATPs for every glucose molecule at the start of the process.

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17
Q

Which organisms need the efficiency to make enough ATP for their needs?

A

Complex organisms.

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18
Q

What happens at the process of oxidative phosphorylation?

A

Pyruvate enters –> mitochondria –> converted into acetyl coA –> fatty acids break down through beta oxidation –> produce acetyl coA –> used by mitochondria –> Acetyl coA joins Krebs cycle.

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19
Q

On what does the amount of coA production depend?

A

On the length of carbon chain.

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20
Q

What happens when the Acetyl coA joins the Krebs cycle?

A

Oxidation is produced.

Co factors are reduced –> fed into –> electron transfer chain.

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21
Q

What is the function of electron transfer chain (ETC)?

A

It hands electrons from one complex to the next.

And it generates ATP.

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22
Q

Which is the final electron acceptor in the ETC?

A

Oxygen.

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23
Q

What is the function of oxygen in ETC?

A

It reacts with H+ –> produces water.

We rely on oxygen.

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24
Q

Which are the three energy sources?

A

Fats.
Carbohydrates in glycogen form.
Amino acids.

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25
Q

What is glycolysis?

A

The initial process of carbohydrate metabolism.

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26
Q

Where does glycolysis occur?

A

In the cytoplasm.

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27
Q

What molecule is really stable on its own and we need to ‘get it going’ through the metabolic pathway?

A

Glucose.

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28
Q

What is the function of glucose?

A

It diffuses easily out of the cell.

Needs to held in place and prevented from escaping.

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29
Q

What is the first step of glycolysis pathway and the total glycolysis pathway?

A

The phosphorylation of glucose –> glucose 6 phosphate (G6P) –> fructose 6 phosphate –> phosphorylation –> fructose 1,6, bisphosphate.

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30
Q

What do the phosphorylation steps use?

A

ATP.

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31
Q

What is the purpose of the phosphorylation steps in the glycolysis pathway?

A

They change the ATP and hormone levels to regulate them.
Example: insulin turn on glycolysis.
Glucagon turns off glycolysis.

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32
Q

How many ATP molecules do we use in the start of the glycolysis pathway?

A

2 ATPs.

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33
Q

How many ATP molecules do we produce at the end of glycolysis pathway?

A

4 ATPs.

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34
Q

What is the net production of ATP in glycolysis for every glycose molecule?

A

2.

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35
Q

What are the advantages of glycolysis?

A

It can directly generate ATP without using oxygen.
It generates NADH to make more ATP.
The rate can be increased quickly.

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36
Q

Is ATP generation in the absence of O2 important?

A

Yes.
It is very important.
If blood supply is high in body areas.
During heavy exercise: sprinting, heart attack, stroke.

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37
Q

When we use glucose as a metabolic fuel, without what can we break it down in the cytoplasm in glycolysis?

A

Without oxygen.

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38
Q

Is the break down of glucose without oxygen in the cytoplasm in glycolysis efficient?

A

No.

It generates lactic acid.

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39
Q

From what are enzyme kinetics altered by?

A

By pH changes.

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40
Q

Where is pyruvate made and during which process?

A

In mitochondria, during glycolysis.

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41
Q

Is the pyruvate generation in the mitochondria during glycolysis more efficient process of Krebs cycle and why?

A

Yes.
It oxidizes carbon metabolites each step –> phosphorylation –> produces 38 ATPs for each glucose.
Underpins all complex life.

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42
Q

What does determine the next step in metabolism?

A

Oxygen levels.

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43
Q

How is the next step in metabolism determined by oxygen levels?

A

Pyruvate is removed.

Or glycolysis stops.

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44
Q

What happens when fatty acid metabolism joins glycolysis pathway?

A

Pyruvate –> converted into –> acetyl coA in mitochondria –> combined with oxygen –> make water + CO2 in Krebs cycle –> Greater ATP synthesis.

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45
Q

In what form does pyruvate can be converted to in yeast and some bacteria?

A

To ehanol.

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46
Q

What happens to pyruvate in humans when no oxygen is available?

A

It is converted to lactate.

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47
Q

What is the Lactate dehydrogenase?

A

An important enzyme.

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48
Q

What is the function of Lactate dehydrogenase enzyme?

A

It reversibly converts pyruvate to lactate and vice versa.

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49
Q

On what does the function of Lactate dehydrogenase enzyme depend on?

A

On how much pyruvate and lactate is present.

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50
Q

Why is the function of Lactate dehydrogenase enzyme important?

A

It maintains glycolysis.

It removes final product of glycolysis.

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51
Q

What happens to our bodies if lactate levels build up?

A

We end up with local acidosis.

Causes cramps.

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52
Q

What must happen to lactate when oxygen becomes available again?

A

It needs to be ‘burned off’.
It is turned back into pyruvate by lactate dehydrogenase.
And enters mitochondria.
And enters Krebs cycle.

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53
Q

What is the Krebs cycle?

A

A pathway.
Glycolysis –> Pyruvate –> used.
Pyruvate –> generates –> NADH + FADH.
NADH +FADH –> used in ETC.

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54
Q

What happens in the presence of oxygen?

A

Pyruvate –> in mitochondria –> converted to key metabolic intermediate: acetyl coA.
Acetyl coA uses CoASH and NAD+.
Carboxyl group is removed from pyruvate –> releases CO2, NAD+ –> reduced to NADH.
Acetyl group –> transferred to co enzyme A.

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55
Q

In what do the products of various steps in Krebs cycle pathways be used?

A

In biosynthesis steps: use carbon backbone.

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56
Q

From what do amino acids can be made?

A

From alpha ketoglutaric acid + oxaloacetic acid.

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57
Q

From what do porphyrins can be made?

A

From succinate.

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58
Q

Where is succinate used?

A

For haemoglobin biosynthesis.

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59
Q

From what can glycose be resynthesized?

A

From malic acid.

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60
Q

What is Acetyl CoA?

A

A key metabolic intermediate.

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61
Q

Where do glycolysis and free fatty acid oxidation lead on?

A

On acetyl-CoA.

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62
Q

From what are ketone bodies made?

A

From acetyl co-A.

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63
Q

When does acetyl co-A makes ketone bodies?

A

When blood glucose is low.

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64
Q

What else can the Krebs cycle generate?

A

The precursors for haem biosynthesis.

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65
Q

Why is Acetyl co-A also a precursor of steroid hormones?

A

Because it is used to make cholesterol from the derived steroids.

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66
Q

Where does fatty acid breakdown lead to?

A

Acetyl coA –> feeds in TCA cycle.

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67
Q

To what are triacyl glycerides hydrolysed?

A

Glycerol + fatty acids.

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68
Q

What happens under tight hormonal control from insulin and other hormones when they are involved in energy balance regulation?

A

Triacyl glycerides are stored in the adipocytes.

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69
Q

How is the process of fatty acid breakdown called?

A

Beta oxidation.

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70
Q

When does beta oxidation occur?

A

In the mitochondria.

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71
Q

How does Beta oxidation start?

A

With an activation phase.

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72
Q

What does the activation phase in Beta oxidation involve?

A

An energizing step.
An ATP consuming reaction.
CoA –> forms acyl Co A.

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73
Q

With what does the energizing step in Beta oxidation similar with?

A

Glycolysis.

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74
Q

What happens in the second step of Beta oxidation?

A

FAD –> reduced to –> FADH2.
Double bond is inserted.
ATP is produced.

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75
Q

How many ATPs are made from 1 fatty acid?

A

1.5 ATPs.

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76
Q

How many ATPs are made from 2 fatty acids?

A

3 ATPs.

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77
Q

What happens in the third step of Beta oxidation?

A

A hydroxyl group is added.

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78
Q

What happens in the fourth step of Beta oxidation?

A

NAD is further reduced to –> NADH.

NADH –> used –> makes –> more ATP.

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79
Q

How many carbons are lost from the carbon chain at each turn of the pathway of Beta oxidation?

A

2 carbons.

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80
Q

What happens to the carbon chain at each turn of the beta oxidation pathway?

A

It gets shorter each time.

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81
Q

What does each cycle of the Beta oxidation pathway produces?

A

An acetyl coA with 3 carbons.

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82
Q

How many ATPs can each acetyl coA make per turn of the Krebs cycle?

A

10 ATPs.

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83
Q

What does the oxidation at each step of Beta oxidation do?

A

It reduces the length of carbon chain.
An it produces acetyl coA.
Acetyl coA –> enters TCA cycle.

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84
Q

Where does the number of acetyl co A molecules made depend on?

A

On the length of the fatty acid chain.

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85
Q

When does Beta oxidation work with fatty acids??

A

When the number of carbons is optimal.

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86
Q

What does Beta oxidation generate?

A

NADH + FADH2.

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87
Q

Where do NADH + FADH2 which are generated by Beta oxidation pathway, used?

A

They are used by ETC.

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88
Q

What do NADH + FADH2 make, when they are generated by Beta oxidation pathway and used by ETC?

A

They make ATP.

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89
Q

Where does amino acid metabolism occur?

A

In the cytoplasm.

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90
Q

How are amino acids derived?

A

From the break down of proteins.

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91
Q

Where can amino acids enter?

A

In the metabolic pathway.

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92
Q

What can amino acids do once they enter the metabolic pathway?

A

Converted to pyruvate.
Or Converted to acetyl coA.
Or feed into the Krebs cycle.

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93
Q

What does the break down of amino acids produces?

A

Nitrogen waste products.

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94
Q

As what do nitrogen waste products present in humans?

A

As urea, excreted as urine.

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95
Q

How many amino acids are turned over by a 70Kg person per day?

A

400g.

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96
Q

How can we replace our loss of nitrogen?

A

By ingesting essential amino acids.

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97
Q

What actually happens in amino acid metabolism?

A

Proteins from muscle or diet –> break down into –> amino acids.
Transamination moves –> amine group of amino acids.
Amine group –> catalysed by aminotransferase specific for amino acid substrate.
Amine group –> stripped off –> leave just carbon skeleton.
Carbon skeleton –> enters metabolic pathway
Example = amine group from alanine –> removed –> produces –> pyruvate.

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98
Q

On what does the entrance of carbon skeleton in metabolic pathway depend?

A

On its structure.

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99
Q

To what are gluconeogenic amino acids converted?

A

To pyruvate.

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100
Q

To what are ketogenic amino-acids converted?

A

To acetyl-CoA.

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101
Q

What happens to acetyl-CoA after it is converted by ketogenic amino acids?

A

Enters Krebs cycle.

Or it is converted to ketone bodies.

102
Q

Why are the metabolic pathways known as catabolic pathways?

A

Because they break down carbon sources.

103
Q

How much ATP is generated in the catabolic pathways of metabolism?

A

Only a small amount.

104
Q

Is ATP used in all steps of metabolic pathways?

A

No.

Only in some steps.

105
Q

What is oxygen in ETC?

A

The final electron acceptor.

106
Q

What is the function of oxygen as the last electron acceptor in ETC?

A

It is combined with H+ –> couples –> break down + oxidative phosphorylation –> make –> ATP –> energy.

107
Q

What is the function of ATP as energy when is generated by carbon hydrogen coupled with oxidative phosphorylation?

A

Powers almost all our essential processes: biosynthesis, movement, ion pumping.

108
Q

Where do the high energy reducing molecules used?

A

In Krebs cycle –> reduction, oxidation.

109
Q

Why do the high energy reducing molecules used in reduction and oxidation steps?

A

To produce ATP.

To link energy consuming pathways of carbon breakdown with energy production.

110
Q

Where is some ATP generated and by what?

A

In the cytoplasm by glycolysis.

111
Q

Where is most of the ATP generated and by what?

A

In the mitochondria.

By oxidative phosphorylation.

112
Q

What happens in oxidative phosphorylation?

A

ADP + substrate –> is converted to ATP in form of carbon chains.
ATP –> generates NADH + oxygen + ADP + Pi (inorganic phosphate).

113
Q

What reaction is oxidative phosphorylation?

A

A redox reaction.

114
Q

Why is oxidative phosphorylation a redox reaction?

A

Because NADH is oxidised.

Oxygen is reduced.

115
Q

What does the generation of ATP requires to be generated?

A

A concentration gradient.

116
Q

What concentration gradient is generated in the generation of ATP?

A

Something like a hydroelectric dam.
Protons.
Or H+.

117
Q

What is the function of hydroelectric dam as concentration gradient?

A

Water is pumped up hill –> released though turbine.

118
Q

Where can the downhill kinetic energy be used to release water though a turbine?

A

Energy –> drives –> turbine –> generates –> electricity.

119
Q

What does the pumping of ATP require?

A

The double membrane of the mitochondria.

120
Q

What happens in the mitochondria in ATP pumping?

A

A sequence of proteins is involved.

121
Q

What do the proteins do in the ATP pumping in mitochondria?

A

Proteins use oxidation of NADH + FADH to pump H+ –> head of protons is released.

122
Q

How is the head of protons released in ATP pumping in mitochondria?

A

In a controlled way.

123
Q

Through what are head protons released?

A

Through the turbine.

124
Q

What is the turbine through which head of protons are released in a controlled way?

A

ATP synthase.

125
Q

Why are the head of protons released in a controlled way through the turbine in ATP binding in mitochondria?

A

To make ATP.

126
Q

Where does the ATP pumping occur?

A

In the mitochondria.

127
Q

How many membranes do mitochondria have?

A

2.

128
Q

What are the membranes of mitochondria?

A

An outer one.

Ans a highly folded inner one.

129
Q

How are the folds called?

A

Cristae.

130
Q

Where are the complexes of the electron transfer chain involved?

A

In ATP generation.

131
Q

Where are the complexes of mitochondria involved?

A

In the inner membrane.

132
Q

Why is the inner membrane of mitochondria so great?

A

Because of the folding.

Lots of complexes are packed into small spaces of mitochondria.

133
Q

Where are the enzymes of Krebs cycle and beta oxidation?

A

In the lumen of the mitochondria.

134
Q

What is the function of the enzymes in Krebs cycle and beta oxidation?

A

To hand their reducing electron carriers to ETC.

135
Q

What is the key feature in mitochondria?

A

The gap between the two membranes.

136
Q

Where do the protons get pumped from the lumen of the mitochondria?

A

In the inter membrane space.

137
Q

Where are the complexes of the ETC embedded?

A

In the inner membrane.

138
Q

What happens every time complexes hand an electron from one complex to the next?

A

One complex is oxidised.
The next is reduced.
A proton = H+ –> pumped into –> intermembrane space.

139
Q

What does the action of complexes in ETC create?

A

A ‘head’ of protons that are itching to get back into the mitochondrion’s lumen down their electrochemical gradient.

140
Q

What do some protons manage to do?

A

To leak back across.

And dissolve energy as heat.

141
Q

What do most of the protons do?

A

Can not leak back.

142
Q

Why do most of the protons can not leak back?

A

Because the membrane of the mitochondrion is relatively impermeable to them.

143
Q

What do most of the protons that can not leak back to the mitochondrion do?

A

They bind with the ‘ratchet’ system of ATP synthase.

144
Q

What is the function of the ‘ratchet’ system of ATP synthase?

A

It allows the protons to cross back into the lumen but by using the ‘proton motive force’.

145
Q

What does the ‘proton motive force do’?

A

It drives ATP synthesis.

146
Q

What is the ATP synthesis?

A

The cellular equivalent of a hydroelectric dam.

147
Q

What do NADH +FADH2 from Krebs cycle and other steps of carbon source breakdown do?

A

They deliver the electrons needed for redox reactions which will occur.

148
Q

What are the NADH + FADH2 based on their function in ETC?

A

Electron carriers.

149
Q

Where do the electrons that are passed from one ETC complex to the next move?

A

From a higher to a lower energy level.

Energetically travelling down hill.

150
Q

What is used to move the H+ from the lumen to the intermembrane space against an electrochemical gradient in ETC?

A

The release of energy.

151
Q

How are the complexes of the ETC labelled?

A

Complexes 1 to 4.

152
Q

What happens at complex 1 of ETC?

A

NADH –> donates –> electrons –> reduces complex.

NADH –> regenerates NAD+ –> returns for use in –> Krebs cycle.

153
Q

Where does the regeneration of NAD+ from NADH occur?

A

In the mitochondrial lumen.

154
Q

Where is the reduction by complex 1 used?

A

In proton pumping across the membrane.

155
Q

What does the complex 2 not do?

A

Pumping protons.

156
Q

Why is the complex 2 important in ETC?

A

Because it receives the electrons donated from FADH2.

157
Q

Are the electrons in FADH2 at a lower energy state than complex 1?

A

Yes.

158
Q

Why do the electrons in FADH2 can not travel uphill to donated them in complex 2?

A

Because they are at a lower energy state than in complex 1.

159
Q

What happens as there are more donated electrons from FADH2?

A

Fewer protons are pumped.

Proton gradient id not built up as much.

160
Q

What is the same function of complex 1 and 2?

A

They hand their electrons on to a carrier molecule.

161
Q

What is the carrier molecule that complex 1 and 2 hand their electrons to?

A

Ubiquinone = Q.

162
Q

What is the ubiquinone molecule?

A

A mobile carrier that slide back and forth electrons.

163
Q

What does the molecule Q do?

A

Picks up electrons from complex 1 and 2.

Delivers the electrons from the complexes to complex 3.

164
Q

What does the complex 3 do?

A

Pumps another H+.

165
Q

What does the H+ pumping of complex 3 allow?

A

The movement of the electrons to another mobile carrier = cytochrome C.

166
Q

What does the mobile carrier cytochrome C from complex 3 do?

A

Delivers the electrons to complex 4.

167
Q

What does complex 4 do?

A

Splits molecular oxygen into 2.

168
Q

What does the molecular oxygen split into 2 by complex 4 do?

A

Accepts H+ in the lumen of mitochondria.

Generates water.

169
Q

How many electrons per oxygen molecule are required?

A

4 electrons.

170
Q

How many water molecules are made per oxygen molecule?

A

2 water molecules.

171
Q

What are the two major jobs of ETC?

A

To turn NADH back into NAD+ and turn FADH2 back into FAD –> to keep catabolic processes of Krebs cycle and fatty acid oxidation going. = biochemical level recycling.
And to generate the proton gradient –> to have ATP.

172
Q

What does the proton motive force is used to do?

A

To drive ATP synthesis through ATP synthase.

173
Q

Where can the uncoupling process be used for?

A

For the proton motive force.

174
Q

How is ATP made?

A

By using the energy form the proton gradient.

175
Q

Why is ATP made?

A

To drive ATP synthesis.

176
Q

How is the process of ATP synthesis called?

A

Chemiosmosis.

177
Q

By what is the gradient that powers ATP synthesis maintained by?

A

By the complexes that make up the ETC.

178
Q

Where is the ATP synthase complex for ATP synthesis embedded in?

A

In the inner membrane of mitochondria.

179
Q

Can the protons pass back through the inner mitochondrial membrane on their own?

A

No.

180
Q

Where are the protons that cannot pass back through the inner mitochondrial membrane on their own trapped in?

A

In the intermembrane space.

181
Q

Why are the protons trapped in the intermembrane space?

A

Because the core of the bilayer membrane is too hydrophobic for ions to get through in large amounts. They need help.

182
Q

In what form does the help come for the protons to pass back through the intermembrane mitochondrial membrane?

A

In the form of ATP synthase.

183
Q

How is the form of ATP synthase called?

A

Complex 5.

184
Q

What is the formation of ATP from ADP?

A

Energetically unfavourable.

Pi + energy –> ADP +Pi –> ATP.

185
Q

What does the ATP synthase do in the formation of ATP from ADP?

A

ATP synthase traps energy from proton gradient –> synthesis.

186
Q

How many subunits occur in ATP synthase?

A

2.

187
Q

What are the subunits of ATP synthase?

A

FO.

F1.

188
Q

What can F1 subunit of ATP synthase do?

A

It rotates in relation to FO.

189
Q

where does the FO subunit of ATP synthase occur?

A

In the membrane.

190
Q

What does the ability to rotate of F1 mean?

A

F1 is a molecular machine.

It is a turbine.

191
Q

From where do the protons move?

A

From a channel in F0 –> bind to a ring on F0.

192
Q

What does the binding of protons on the ring of F0 cause?

A

F0 to rotate a notch.

193
Q

What do H+ ions do?

A

They exit from F0 –> in lumen.

194
Q

What is the exist of H+ from F0 into lumen?

A

A one way door.

195
Q

Where are the H+ transferred from the lumen?

A

It is transferred to F1 subunit.

196
Q

By what is the H+ transferred from the lumen to F1 subunit?

A

By a central stalk.

197
Q

What does the central stalk do?

A

It connects the F1 and F0 subunits of ATP synthase.

198
Q

What is the shape of the stalk?

A

It is shaped like a cam shaft.

199
Q

What happens to the stalk as it rotates?

A

It squashes F1 subunit –> conformational change in F1.

200
Q

Of what is F1 made?

A

Of 3 dimers.

201
Q

In what are the 3 dimers of F1 arranged?

A

In a ring.

202
Q

What happens in ATP synthesis process?

A

ADP + P1 bind in gap between two dimers –> stalk rotation –> dimers squash together –> squash ADP + Pi together –> ADP +Pi fuse –> form ATP.

203
Q

What does the other rotation of the stalk that is driven by H+ movement through F0 do?

A

It lets dimers pop apart again –> release newly formed ATP –> ADP +Pi bind again.

204
Q

What does hold the 2 subunits together and allows the dimers to flex with each rotation of the internal stalk?

A

A flexible peripheral stalk.

205
Q

What process gives the inner mitochondrial membrane its characteristic folds = cristae?

A

Dimerization of ATP synthase.

206
Q

What happens in the dimerization of ATP synthase?

A

The proton gradient is focussed near ATP synthase –> makes process highly efficient.

207
Q

In what does the top of ATP synthase complex rotate in?

A

In small protons passing through.

208
Q

How many rotations of ATP synthase required to produce 1 ATP?

A

3.

209
Q

What does maintain the H+ in ETC?

A

Other complexes.

210
Q

What does the proton gradient do?

A

It couples oxidation of fuels.

211
Q

Why does the proton gradient couples oxidation of fuels?

A

To phosphorylate ADP –> produce chemical energy –> form ATP.

212
Q

What is the process of: H+ + oxidation of fuels –> ADP phosphorylation –> chemical energy –> ATP called?

A

The proton motive force.

213
Q

What else can the proton motive force do?

A

Active transport.

214
Q

What is the process of active transport of proton motive force?

A

Pyruvate enters –> mitochondria.
ADP enters –> mitochondria.
ATP exits –> mitochondria –> used by cytoplasmic enzymes.

215
Q

What drives ADP-ATP exchange?

A

A voltage gradient.

216
Q

What drives the pyruvate and phosphate import?

A

pH gradient.

217
Q

What do the complexes do in prokaryotes?

A

They set up a proton pump between the cytoplasm and the intermembrane space between outer bacterial membrane and inner membrane = in a mitochondrion.

218
Q

What can the complexes in prokaryotes do?

A

They use the flow of protons –> drive flagella movement.

219
Q

The process of complexes that set up proton pump in the mitochondrion to use the flow of protons to drive flagella movement describes?

A

How the proton gradient is used to drive the motor of F0 and F1 in ATP synthase.

220
Q

What is the difference between ATP synthesis process and complexes process in prokaryotes?

A

The energy is directed in –> movement.

Or the energy is directed in –> kinetic energy.

221
Q

In how many revolutions does flagellar motor rotate?

A

> 100/second.

222
Q

What protons occur in flagellum?

A

Stator proteins.

And rotor proteins.

223
Q

Where does ETC result in?

A

In a build up of protons in the intermembrane space in mitochondria.

224
Q

For what is the head of protons used?

A

To drive ATP synthesis through ATP synthase.

225
Q

What occurs across the membrane normally?

A

A ‘proton leak’.

226
Q

What doe the ‘proton leak’ do?

A

It dissolves energy as heat.

It helps endotherms –> generate own body heat.

227
Q

Who have lower proton leak. Reptiles, mammals or birds?

A

Reptiles.

228
Q

What else do we have in BAT?

A

UCP1.

229
Q

What is UCP1?

A

A protein.

230
Q

What does UCP1 do when activated?

A

It allows protons to move back rapidly –> generate heat, not ATP.

231
Q

Why is UCP1 process important?

A

It is a fast method.

It maintains body T when we get cold.

232
Q

What would happen if all our cells moves protons back rapidly and generate heat than ATP?

A

We would die from ATP lack.

233
Q

Where is the UCP1 process done?

A

In specialised cells.

234
Q

Why is UCP1 process carefully regulated?

A

For the cells to not lose ATP generating capacity altogether.

235
Q

What was used to be believed for BAT depots between shoulder blades?

A

Only occurred in new-borns –> regulate T after birth while other aspects of thermal balance were developing.

236
Q

What is ‘hibernoma’?

A

An unusual cancer form found in 2009.

237
Q

What were scientists using to find the tumours in ‘hibernoma’ cancer in 2009?

A

A whole-body image that identifies regions of high glucose uptake.

238
Q

What did scientists discovered about ‘hibernoma’ cancer in 2009?

A

People without cancers had lots of little diffuse ‘bright spot’ throughout their fat tissue.
Adult humans have BAT = harder to find than in babies.

239
Q

What did scientists discovered about ‘hibernoma’ cancer in 2009?

A

People without cancers had lots of little diffuse ‘bright spot’ throughout their fat tissue.
Adult humans have BAT = harder to find than in babies.

240
Q

Why is harder to find BAT in adults than in babies?

A

Because depots are small, scattered, not predictable in location between people .
Depots only activate when the person is cold.

241
Q

Where is BAT most predictable?

A

Under clavicles in neck.

242
Q

Why was WAT ‘browned up’?

A

To help people lose fat mass.

243
Q

What is BAT?

A

Brown adipose tissue.
Highly vascularised.
Lots of mitochondria for heat production.

244
Q

What is WAT?

A

White adipose tissue.
Few mitochondria.
Specialised for fat storage.

245
Q

What is UCP1?

A

Uncoupling protein.

246
Q

What was dinitrophenol = DNP in 1930?

A

A chemical.

A powerful weight loss drug.

247
Q

How did DNP work?

A

By uncoupling ETC from ATP synthesis.

Collapsing proton gradient in uncontrolled way.

248
Q

What were the serious effects from DNP drug?

A

Hyperthermia.

249
Q

Why was hyperthermia caused by DNP drug?

A

Because energy –> drives ATP production –> BUT –> was dissolved as heat.

250
Q

What is he inability to control the ATP production means?

A

Cells no longer produce enough energy in ATP form.

Cells generate too much heat.

251
Q

Is the DNP drug still legal?

A

No.

It can be purchased illegally.

252
Q

What happens to people that buy DNP drug illegally?

A

Uncontrolled uncoupling of oxidation from phosphorylation –> death.