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Z OLD ESA 1- Metabolism > Energy production- Carbohydrate > Flashcards

Energy production- Carbohydrate Flashcards

1
Q

What common product are glucose, fatty acids and alcohol broken down into?

A

Acetyl CoA

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2
Q

What is glucose converted into prior to Acetyl CoA?

A

Pyruvate

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3
Q

What else can be converted into Acetyl CoA?

A

Keto-acids

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4
Q

Where do keto-acids come from?

A

The break down of amino acids

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5
Q

What is the advantage of amino acids, glucose, fatty acids and alcohol all being capable of conversion into Acetyl CoA?

A

It allows for interconversion

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6
Q

What is acetyl CoA ultimately converted too?

A

CO 2

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7
Q

Other than keto-acids, what can amino acids be converted into?

A

NH 3

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8
Q

What is NH 3 ultimately converted into?

A

Urea

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9
Q

What are the 4 stages of catabolism?

A
  • Breakdown to building block materials
  • Breakdown of metabolic intermediates
  • TCA (Kreb’s cycle) and release of reducing power and energy
  • Oxidative phosphorylation and conversion of reducing power into ATP
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10
Q

What is the purpose of breaking food down into building block materials?

A

To convert nutrients to a form that can be taken up by cells

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11
Q

Where does breaking down of substances into building blocks occur?

A

Extracellular, in the GI tract, technically outside of the body

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12
Q

How do the building block materials get into the body?

A

They are absorbed by epithelial cells in the GI tract

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13
Q

What happens to building block materials once they have been absorbed by epithelium in the GI tract?

A

They are bought into circulation for use

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14
Q

What is necessary for absorption of building block materials by the GI tract?

A

Transport mechanisms in the membrane

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15
Q

Does breaking down into building block materials release energy?

A

No

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16
Q

What bonds are broken when producing building block materials?

A

C-N and C-O

No C-C

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17
Q

Isbreakdown into metabolic intermediates and release of reducing power intracellular or extracellular?

A

NAME?

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18
Q

What cells does breakdown into metabolic intermediates and release of reducing power occur in?

A

Cells at target organs

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19
Q

Is breakdown into metabolic intermediates and release of reducing power a cytosolic or mitochondrial process?

A

Can be both

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20
Q

What is the result of some reactions in the breakdown into metabolic intermediates and release of reducing power being packaged away?

A

Gives control over synthesis and catabolism

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21
Q

Isbreakdown into metabolic intermediates and release of reducing power oxidative or reductive?

A

NAME?

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22
Q

What is the result ofbreakdown into metabolic intermediates and release of reducing power being oxidative?

A

It requires coenzymes

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23
Q

What happens to to coenzymes used inbreakdown into metabolic intermediates and release of reducing power after?

A

They are reduced

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24
Q

Is energy produced duringbreakdown into metabolic intermediates and release of reducing power?

A

A small proportion is

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25
Q

How is ATP produced duringbreakdown into metabolic intermediates and release of reducing power?

A

Direct phosphorylation of ADP to ATP

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26
Q

What bonds are broken inbreakdown into metabolic intermediates and release of reducing power?

A

C-C

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27
Q

Where does the TCA occur?

A

In the mitochondria

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28
Q

Is the TCA oxidative or reductive?

A

NAME?

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29
Q

What is the result of TCA being oxidative?

A

It requires NAD + and FAD

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30
Q

Is energy produced in the TCA cycle?

A

A small proportion is produced directly

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31
Q

What happens to acetyl in the TCA cycle?

A

It is converted to 2CO 2

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32
Q

What has happened in the conversion of acetyl to 2CO 2 ?

A

Carbon has been oxidised

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33
Q

What happens to the CO 2 produced in the TCA cycle?

A

It is put back in circulation, then breathed out at lungs

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34
Q

What does the TCA produce?

A

Precursors for biosynthesis

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35
Q

What is the advantage of the TCA producing intermediates?

A

It’s a way of interconnecting pathways

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36
Q

Where does oxidative phosphorylation occur?

A

In the mitochondria

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37
Q

What happens in oxidative phosphorylation?

A

Electron transport and ATP synthesis

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38
Q

What happens to NADH and FADH 2 in oxidative phosphorylation?

A

They are re-oxidised

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39
Q

Why are NADH and FADH 2 re-oxidised in oxidative phosphorylation?

A

The energy within them in used to drive ATP synthesis

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40
Q

What is required for oxidative phosphorylation?

A

Oxygen

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41
Q

What happens to oxygen in oxidative phosphorylation?

A

It is reduced to H 2 O

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42
Q

Why is O 2 reduced in oxidative phosphorylation?

A

Needed to oxidise H carriers

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43
Q

Does oxidative phosphorylation produce energy?

A

Yes, large amounts of ATP are produced

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44
Q

What is the general formula of carbohydrates?

A

(CH 2 O) n

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45
Q

What are the two types of sugars?

A
  • Aldose

- Ketose

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46
Q

What is an aldose sugar?

A

One that contains a aldehyde group

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47
Q

What is a ketose sugar?

A

One that contains a ketogroup

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48
Q

Are sugars hydrophilic or hydrophobic in nature?

A

Quite hydrophilic

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49
Q

Why are sugars quite hydrophilic in nature?

A

They have multiple -OH groups

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50
Q

What is a monosaccharide?

A

A single unit

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51
Q

How many C’s are in a monosaccharide?

A

03-Sep

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52
Q

What is a triose sugar?

A

A 3 carbon sugar

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53
Q

What is a pentose sugar?

A

A 5 carbon sugar

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54
Q

What is a hexose sugar?

A

A 6 carbon sugar

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55
Q

How do monosaccharides with more than 5 carbons generally exist?

A

In a ring structure

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56
Q

Why do monosaccharides with more than 5 C atoms generally exist in a ring structure?

A

Because keto/aldehyde group at one end comes round and interacts with the other end, which cyclises the molecule

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57
Q

What reaction is occurring when a ring is formed in a sugar?

A

Carbonyl reacts with alcohol group

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58
Q

Give 3 features of hydrophilic molecules

A
  • Attract water
  • Water soluble
  • Don’t pass across the cell membrane without transporters
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59
Q

What is meant by sugars being partially oxidised?

A

They have H on them

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60
Q

What is the result of sugars being partially oxidised?

A

They need less oxygen than fatty acids for complete oxidation

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61
Q

What is a disaccharide

A

A molecule composed of two monosaccharides

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62
Q

What is oligosaccharide?

A

A molecule with 3-12 monosaccharides

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63
Q

Give an example of a group of oligosaccharides

A

Dextrins

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64
Q

What are polysaccharides?

A

Molecules with 10-100 monosaccharide units

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65
Q

What kind of bond is formed between monosaccharides?

A

O-glycosidic bond

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66
Q

What happens when an O-glycosidic bond is formed?

A

Water is eliminated

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67
Q

What are the two kinds of O-glycosidic bonds?

A

NAME?

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68
Q

What is the difference between alpha and beta glycosidic bonds?

A

The alpha bond sticks up, and the beta bond goes down

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69
Q

Why is wether you have an alpha or beta glycosidic bond important?

A

Because enzyme function depends on bond type

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70
Q

What is the main storage polysaccharide in animals?

A

Glycogen

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71
Q

Where is glycogen stored?

A

Liver and muscles

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72
Q

What is the purpose of glycogen?

A

It is a rapidly mobilisable energy store

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73
Q

What bonds are found in glycogen?

A
  • Alpha 1-4

- Alpha 1-6

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74
Q

Why are the two different bond types in glycogen?

A

It produces branches

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75
Q

How are glucose molecules organised in glycogen?

A

They are largely lined up end on end

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76
Q

Why is glycogen used as the store, not glucose?

A

Takes highly osmotic glucose effectively out of the solution

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77
Q

What is the main glucose polymer in plants?

A

Starch

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78
Q

What is starch made up of?

A

A mixture of amylose and amylopectin

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79
Q

What is the bond type in amylose?

A

Alpha 1-4

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80
Q

What are the bond types in amylopectin?

A
  • Alpha 1-4

- Alpha 1-6

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81
Q

How does starch differ from glycogen?

A

Less highly branched

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82
Q

What is starch broken down into in the GI tract?

A

NAME?

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83
Q

What is cellulose?

A

A structural glucose polymer in plants

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84
Q

What bonds are present in cellulose?

A

Beta 1-4

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85
Q

What is the difference between beta 1-4 and alpha 1-4 linkages?

A

Beta are more stable

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86
Q

Why can’t cellulose be digested?

A

There are no GI enzymes to digest ß1-4

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87
Q

What is cellulose important for?

A

GI function

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88
Q

Why is cellulose important for GI function?

A

Provides substrate for other molecules to stick to, to be acted on my other enzymes

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89
Q

What is the body content of dietary carbohydrate?

A

1%

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90
Q

Other than dietary, what are the other sources of carbohydrate?

A

It can be synthesised from amino acids

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91
Q

Where does carbohydrate digestion occur?

A

GI tract (extracellular)

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92
Q

What happens in the digestion of carbohydrate?

A

Hydrolysis of glycosidic bonds

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93
Q

Give 3 places that produce enzymes that are required for carbohydrate digestion

A
  • Salivary glands
  • Pancreas
  • Small intestine
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94
Q

What enzyme is present in saliva?

A

Amylase

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95
Q

What does amylase do?

A

Breaks down starch and glycogen into dextrins by cleaving alpha1-4 glycosidic bonds

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96
Q

What enzyme for carbohydrate digestion does the pancreas produce?

A

Amylase

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97
Q

Is pancreatic amylase the same as salivary amylase?

A

No, but has same function

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98
Q

What does pancreatic amylase do?

A

Breaks carbohydrates down into monosaccharides

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99
Q

What enzymes for carbohydrate digestion does the small intestine have?

A

It has the disaccharidases lactase, sucrase, pancreatic amylase and isomaltase

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100
Q

Where are the enzymes in the small intestine?

A

Attached to the brush border membrane of epithelial cells

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101
Q

What does lactase break down?

A

Lactose

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102
Q

What does sucrase break down?

A

Sucrose

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103
Q

What does isomaltase break down?

A

Alpha1-6 branches

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104
Q

What happens in absorption?

A

Active transport into intestinal epithelial cells

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105
Q

How do monosaccharides get to the target tissues?

A

Via the blood supply

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106
Q

Why does absorption need active transport?

A

Because the concentration in the cells is greater than that in the lumen

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107
Q

How is glucose uptaken into the cells?

A

Facilitated diffusion

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108
Q

What allows facilitated diffusion of glucose?

A

The transport proteins GLUT1-GLUT5

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109
Q

What is the difference between each GLUT?

A

They have different tissue distribution and affinities

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110
Q

How can GLUT transporters be controlled?

A

Hormonally

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111
Q

Which cells can metabolise glucose?

A

All

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112
Q

Why can all cells metabolise glucose?

A

They all have the glycolytic pathway

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113
Q

Which tissues have an absolute requirement for glucose?

A
  • RBC
  • WBC
  • Kidney medulla
  • Lens of eye
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114
Q

What does the uptake of glucose to tissues with an absolute glucose requirement depend on?

A

The concentration of glucose in the blood

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115
Q

When are obligate glucose uses susceptible?

A

In starvation

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116
Q

What happens in starvation conditions?

A

The body goes to great lengths to maintain glucose in these tissues, so they have a continuing substrate supply

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117
Q

What tissues prefer glucose as their substrate supply?

A

CNS (brain)

However, they are not obligated

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118
Q

Which tissues need glucose for specialised functions?

A

NAME?

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119
Q

Why do the liver and adipose tissue require glucose for specialised functions?

A

They require carbohydrate backbone for more complex lipid molecule synthesis

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120
Q

What is the central pathway in CHO metabolism?

A

Glycolysis

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121
Q

Where does glycolysis occur?

A

In the cytoplasm of all cells

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122
Q

What are the functions of glycolysis?

A
  • Oxidise glucose
  • NADH (reducing equiv.) production
  • Synthesis of ATP from ADP
  • Produce C 3 and C 6 intermediates
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123
Q

Is glycolysis exergonic or endergonic?

A

Exergonic

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124
Q

Is glycolysis oxidative or reductive?

A

Oxidative

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125
Q

Is there any loss of C in glycolysis?

A

No, it’s just cut in half

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126
Q

Can glycolysis operate anaerobically?

A

Yes, with one additional enzyme

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127
Q

When will glycolysis need to operate anaerobically?

A

When blood supply does not keep up with metabolic need for O 2

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128
Q

Give the overall equation for glycolysis

A

Glucose (C6) + 2Pi + 2ADP + 2NAD + → 2 Pyruvate (C3) + 2ATP + 2NADH + 2H + + 2H 2 O

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129
Q

What is required for each step of the glycolytic pathway?

A

Specific enzymes

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130
Q

What is the first step of glycolysis?

A

Phosphorylation of glucose to form glucose-6-phosphate

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131
Q

What happens in the phosphorylation of glucose?

A

Phosphate is transferred from ATP to glucose

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132
Q

Why does glucose need to be phosphorylated in glycolysis?

A

It needs to be activated, otherwise glucose is a stable molecule

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133
Q

What is the result of the phosphorylation of glucose?

A

NAME?

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134
Q

How much ATP does step 1 of glycolysis use?

A

2 moles per mole of glucose

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135
Q

What happens in step 2 of glycolysis?

A

Isomerisation- G-6-P is rearranged to form fructose-6-P

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136
Q

What happens in step 3 of glycolysis?

A

F-6-P phosphorylated to form F-1,6-bisP

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137
Q

What is the purpose of the phosphorylation of F-6-P?

A

It activates the molecule, so it becomes much more energetic

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138
Q

Which steps in phase 1 of glycolysis (steps 1-3) are committing?

A

1 and 3

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139
Q

Why are steps 1 and 3 of glycolysis committing?

A

They have a large negative ∆G

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140
Q

At what step is glucose committed to metabolism via glycolysis?

A

3

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141
Q

What is the result of step 3 committing glucose to metabolism by glycolysis?

A

It can be used as a regulatory step

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142
Q

What happens in reaction 4 of glycolysis?

A

Cleavage of C 6 to C 3

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143
Q

What is formed in the cleavage of C 6 to C 3 ?

A

DHAP and G-3-P

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144
Q

What is reaction 5 of glycolysis

A

DHAP ↔ G-3-P

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145
Q

What happens in reaction 6 of glycolysis?

A

A small amount of reducing power is captured in NADH

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146
Q

How is reducing power captured in reaction 6 of glycolysis?

A

By coupling to oxidation reactions

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147
Q

What happens in reaction 7-10 of glycolysis?

A

ATP synthesis

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148
Q

Why can ATP synthesis occur in stages 7-10 in glycolysis?

A

Because the molecules are now energetic enough to give up energy

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149
Q

What kind of phosphorylation occurs in steps 7-10 of glycolysis?

A

Substrate level phosphorylation

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150
Q

How does substrate level phosphorylation occur in steps 7-10 of glycolysis?

A

1,3-BPG and ADP are bought together in an enzymes active site, where direct phosphate transfer occurs

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151
Q

Which reaction of 7-10 of glycolysis is irreversible?

A

10

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152
Q

Why is reaction 10 of glycolysis irreversible?

A

Because it has a large negative ∆G

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153
Q

What does the body want to do in times of starvation?

A

Make glucose

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154
Q

What can be used to make glucose in times of starvation?

A

Some of the enzymes in the glycolytic enzymes

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155
Q

What must be done to use the glycolytic pathway to produce glucose?

A

Must find ways of bypassing steps 1,3 and 10

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156
Q

Why must steps 1, 3 and 10 by bypassed when making glucose using the glycolytic pathway?

A

Because the reactions are so energetically committed

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157
Q

How much ATP is synthesised during glycolysis?

A

Net 2 moles of ATP per mole of glucose- 2 moles are invested to get it going, and 4 moles are produced per mole of glucose (C 3 x 2)

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158
Q

Why does glycolysis occur in small steps?

A
  • Chemistry easier in small steps
  • Efficient energy conversion
  • Gives versatility
  • Can be controlled
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159
Q

Why does smaller steps mean more efficient energy conversion?

A

If large, complex molecules used, more energy is wasted as heat

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160
Q

Why does smaller steps give more versatility in glycolysis?

A

NAME?

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161
Q

Where is DHAP formed in glycolysis?

A

In step 4, when C 6 is cleaved into 2 x C 3 , one of which is DHAP

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162
Q

What is DHAP converted into?

A

Glycerol phosphate

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163
Q

Give the equation for the conversion of DHAP to glycerol phosphate

A

DHAP + NADH→ Glycerol Phospate + NAD +

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164
Q

What enzyme is required for the conversion of DHAP to glycerol phosphate?

A

Glycerol 3-phosphate dehydrogenase

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165
Q

What kind of molecule is glycerol phosphate?

A

A 3 carbon phosphorylated alcohol

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166
Q

Where is glycerol phosphate important?

A

In triglyceride and phospholipid biosynthesis

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167
Q

Why is glycerol phosphate important in triglyceride synthesis?

A

It forms the backbone

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168
Q

Where is glycerol phosphate produced?

A
  • Adipose tissue

- Liver

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169
Q

What is the result of DHAP being required for lipid synthesis in liver?

A

Lipid synthesis in liver requires glycolysis

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170
Q

Can the liver phosphorylate glycerol directly?

A

Yes

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171
Q

What is 1,3-bisphosphoglycerate converted into?

A

2,3-bisphosphoglycerate

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172
Q

What enzyme is required for the conversion of 1,3-BPG to 2,3-BPG?

A

Bisphosphoglycerate mutase

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173
Q

What can 2,3-BPG interact with?

A

Haemoglobin

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174
Q

Why can 2,3-BPG interact with haemoglobin?

A

Because it is negatively charged, so can interact with positive charges within haemoglobin

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175
Q

How is 2,3-BPG produced in red blood cells?

A

From 1,3-BPG

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176
Q

Why is 2,3-BPG important?

A

Important regulator of oxygen affinity in haemoglobin- produces the tense form

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177
Q

What concentration is 2,3-BPG present in red blood cells?

A

5mM- same as haemoglobin

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178
Q

What does transfusion blood contain to provide the 2,3-BPG required?

A

Glucose

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179
Q

How long can transfusion blood be kept for?

A

120 days

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180
Q

Why can transfusion blood only be kept for 120 days?

A

Any longer and the 2,3-BPG all gets metabolised

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181
Q

What are the 2 regulation methods for glycolysis?

A

NAME?

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182
Q

How does metabolic regulation of glycolysis occur?

A

If high [NADH] (therefore low [NAD + ], signals high energy levels, which causes product inhibition at step 6, which thereby inhibits glycolysis

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183
Q

How does high [NADH] cause product inhibition at step 6 of glycolysis?

A

If the product of the enzyme is high, it will feed back into the equilibrium, pushing the reaction in the opposite direction

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184
Q

How does the product inhibition at step 6 cause an overall inhibition of glycolysis?

A

If glucose comes in at the top of the pathway, the whole pathway backs up because the concentration of substrates increases, which allows G-6-P to reach a concentration that means it’s fed into glycogen storage

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185
Q

Where would you not use regulation on enzymes?

A

In a reaction that comes to equilibrium

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186
Q

Why would you not put regulation on a reaction that comes to equilibrium?

A

It would still come to the same equilibrium, just reach it at a different rate, so no regulation

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187
Q

Which enzymes are potential sites of control in metabolic pathways?

A

Those catalysing essentially irreversible reactions

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188
Q

What are the two methods of enzymatic regulation in glycolysis?

A

NAME?

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189
Q

What happens in allostery?

A

The activator/inhibitor binds at ‘another’ site

190
Q

What two sites do proteins have?

A
  • Catalytic site

- Regulatory site

191
Q

What happens at the catalytic site?

A

The substrate is converted to products

192
Q

What happens at the regulatory site?

A

The binding of a specific regulatory molecule

193
Q

What effect does the binding of a specific regulatory molecule have?

A

It can change the conformation of a protein, changing the catalytic activity

194
Q

Does the binding of allosteric molecules have a inhibitory or activating effect?

A

Can be either

195
Q

What happens in covalent modification of enzymes?

A

Phosphorylation or dephosphorylation

196
Q

What enzymes are affected in the allosteric regulation of glycolysis?

A

NAME?

197
Q

How is hexokinase affected by allosteric inhibition?

A

Decreased by G-6-P

198
Q

How does allosteric inhibition using hexokinase in glycolysis work?

A

Hexokinase has a second, allosteric site that recognises G-6-P, so when G-6-P levels increase, causes product inhibition.

199
Q

What is the significance of phosphofructokinase-1?

A

It is the enzyme that is responsible for the committing step in glycolysis

200
Q

How is phosphofructokinase-1 affected by allosteric regulation in the muscle?

A

It is decreased by high ATP:AMP ratio

201
Q

How does allosteric activation using phosphofructokinase-1 in the muscle work?

A

The enzyme is stimulated by AMP as it binds as a positive allosteric regulator

202
Q

What is the importance of AMP being a positive allosteric regulation onphosphofructokinase-1?

A

AMP is the low energy signal, as ATP is converted to ADP and AMP, so activates enzyme to make more energy when it’s low

203
Q

What happens tophosphofructokinase-1 in times of high energy?

A

There is feedback inhibition from ATP, so negative feedback on committing enzyme

204
Q

How is phosphofructokinase-1 affected by allosteric regulation in the liver?

A

It is increased by high insulin:glucagon ratio

205
Q

How is pyruvate kinase affected by allosteric regulation?

A

Increased by high insulin:glucagon

206
Q

Why is pyruvate kinase increased by high insulin:glucagon

A

It tells the cell that there is lots of glucose present, so the high ratio means that the enzyme can be switched on to use the glucose

207
Q

How is pyruvate kinase switched on?

A

Dephosphorylation

208
Q

What would happen if NAD + was not regenerated from NADH produced during glycolysis?

A

Glycolysis would stop due to product inhibition at step 6

209
Q

How many moles of NADH are produced per mole of glucose?

A

2

210
Q

What is NAD + essential for?

A

The continuation of the glycolytic pathway

211
Q

How does the cumulative level of NAD + and NADH change?

A

It doesn’t, it remains constant

212
Q

When is NAD + usually regenerated from NADH?

A

In stage 4 of metabolism

213
Q

When can stage 4 of metabolism not occur?

A

NAME?

214
Q

Why can’t RBC’s regenerate NAD + from NADH?

A

Because they have no stage 3 and 4 of metabolism

215
Q

Where is the oxygen supply often reduced?

A

To the gut and the muscles

216
Q

How can NAD + be regenerated when stage 4 of metabolism cannot occur?

A

Using lactate dehydrogenase (LDH)

217
Q

Give the equation for the regeneration ofNAD + using LDH

A

NADH + H + + pyruvate ↔ NAD + + lactate

218
Q

What is the problem with the regeneration ofNAD + using LDH?

A

It produces an acid

219
Q

What must be done to the lactate?

A

It must be removed

220
Q

Why must the lactate be removed?

A

Otherwise muscles would fatigue

221
Q

Where is lactate predominantly produced?

A

NAME?

222
Q

What happens to the lactate produced in tissues?

A

It is released into blood

223
Q

Where is lactate normally metabolised?

A

Liver and heart

224
Q

How is lactate usually metabolised?

A

Using LDH, processed by the reverse reaction

225
Q

What must happen in the liver and heart for efficientNAD + regeneration?

A

Must be well supplied with oxygen

226
Q

In what 3 ways is lactate utilised?

A

NAME?

227
Q

Give the equation for the conversion of lactate into pyruvate

A

NAD + + lactate → NADH + H + + pyruvate

228
Q

Where is lactate used directly for energy production?

A

In the heart

229
Q

How is lactate used directly for energy production in the heart?

A

Through the Krebs cycle and oxidative phosphorylation

230
Q

What is the ultimate product from the use of lactate to produce energy directly?

A

CO 2

231
Q

Where does the conversion of lactate to glucose occur?

A

The liver

232
Q

What is the process of converting lactate to glucose called?

A

Gluconeogenesis

233
Q

Give 4 situations where the conversion of lactate to glucose is impaired

A
  • Liver disease
  • Thiamine deficiency
  • Alcohol
  • Enzyme deficiencies
234
Q

Why is gluconeogenesis inhibited after alcohol?

A

Because alcohol is metabolised by alcohol dehydrogenase, which takesNAD + and converts it to NADH, thereforeNAD + can’t be used for reconverting to lactate

235
Q

How is lactate produced via pyruvate?

A

Using glucose and alanine

236
Q

How much lactate is produced without major exercise?

A

40-50g per 24hrs

237
Q

How much lactate is produced with strenuous exercise?

A

30g within 5mins

238
Q

What can lactate production in pathological situations lead too?

A

Shock or congestive heart failure

239
Q

When may pathological lactate production occur?

A

When circulation is compromised to normally oxygenated tissues

240
Q

What 3 factors determine the plasma concentration of lactate?

A
  • Production
  • Utilisation
  • Kidneys
241
Q

Which tissues utilise lactate

A

Liver, heart and muscle

242
Q

What disposes of lactate?

A

Kidneys

243
Q

At what plasma concentration of lactate would a patient have hyperlactaemia?

A

2-5mM

244
Q

Is hyperlactaemia above or below the renal threshold?

A

Below

245
Q

Does hyperlactaemia cause a change in blood pH?

A

No

246
Q

Why does hyperlactaemia not cause a change in blood pH?

A

Because there is sufficient circulating protein to buffer blood pH

247
Q

At what plasma concentration of lactate would a patient have lactic acidosis?

A

Above 5mM

248
Q

Is lactic acidosis above or below the renal threshold?

A

Above

249
Q

What happens to the blood pH in lactic acidosis?

A

It decreases

250
Q

What is fructose converted to in the body?

A

2 molecules of G-3-P

251
Q

What is galactose converted to in the body?

A

G-1-P, then to G-6-P, then G-3-P

252
Q

What happens to all carbohydrate in the diet?

A

It ultimately goes to glycolysis to be metabolised

253
Q

Where does fructose in the diet come from?

A

Cane/beet sugar

254
Q

What is sucrose a disaccharide of?

A

Fructose + glucose

255
Q

Where is fructose metabolised?

A

In liver

256
Q

What kind of enzymes metabolise fructose?

A

Soluble

257
Q

Describe the metabolism of fructose

A
  • Fructose converted into fructose-1-P, through the action of fructokinase. Requires ATP
  • Fructose-1-P is converted into 2-glyceraldehyde-3-P, by action of aldolase.
  • 2-glyceraldehyde-3-P goes into glycolysis
258
Q

What conditions can arise from errors in fructose metabolism?

A
  • Essential fructosuria

- Fructose intolerance

259
Q

What is missing in essential fructosuria?

A

Fructokinase

260
Q

What happens in essential fructosuria?

A

Fructose levels build in circulation, rising to a level that is greater than the renal threshold

261
Q

What is the clinical presentation of essential fructosuria?

A

Fructose in urine, but no clinical signs

262
Q

What is missing in fructose intolerance?

A

Aldose

263
Q

What happens to fructose metabolism in fructose intolerance?

A

Fructose can feed into the pathway and form F-1-P, but this cannot be metabolised, causing accumulation in the liver

264
Q

What is the result of the accumulation of F-1-P in the liver?

A

Causes liver damage

265
Q

What is the treatment for fructose intolerance?

A

Remove fructose from diet

266
Q

Where does galactose come from?

A

Milk

267
Q

What is lactose a disaccharide of?

A

Glucose + galactose

268
Q

Where is galactose metabolised?

A

Liver

269
Q

Describe the metabolism of galactose

A
  • Galactose is converted into galactose-1-P, by action of galactokinase. This requires ATP.
  • Galactose-1-P is converted into glucose-1-P, by action of galactose-1-P uridyl transferase. This reaction also causes conversion of UDP-glucose to UDP-galactose, by action of UDP-galactose 4’-epimerase
  • Glucose-1-P goes into glycolysis
270
Q

What does UDP-galactose 4’-epimerase do?

A

Mutagensies galactose to glucose by moving hydroxyl groups around

271
Q

What is the role of UDP-glucose in galactose metabolism?

A

It acts catalytically

272
Q

What is the clinical importance of galactose metabolism?

A

Galactosaemia

273
Q

What can cause an inability to utilise galactose?

A
  • Galactokinase deficiency

- Transferase deficiency

274
Q

Is galactokinase deficiency rare or common?

A

Rare

275
Q

What happens in galactokinase deficiency?

A

Galactose accummulates

276
Q

Is transferase deficiency rare or common?

A

Common

277
Q

What happens in transferase deficiency?

A

Galactose and galactose-1-P accumulate

278
Q

What happens when galactose levels rise?

A

Can reach concentrations that enter enzymes that have low Km for galactose, and therefore wouldn’t normally metabolise galactose

279
Q

Give an example that only metabolises galactose when it’s concentrations get too high

A

Aldose reductase

280
Q

Give the equation for the effect of aldose reductase on galactose

A

Galactose + NADPH → Galactitol + NADP +

281
Q

What is the result of the depletion of NADPH levels?

A

It damages structures

282
Q

Why does NADPH depletion cause structure damage?

A

It prevents maintenance of sulphydryl groups on proteins, leading to inappropriate disulphide bond formation

283
Q

What is the result of the inappropriate formation of disulphide bonds?

A

The loss of structural and functional integrity of some proteins that depend on free -SH groups

284
Q

What can happen to proteins that rely on free -SH groups?

A

Protein clumping and damage to cells

285
Q

Give a specific example of problems caused by failure to maintain free -SH groups

A

In the lens of the eye

286
Q

What happens in the lens of the eye when free -SH groups not maintained?

A

Get inappropriate cross linking in the eye, leading to cataracts

287
Q

What organs does the accumulation of galactose-1-P affect?

A

Kidneys, liver and brain

288
Q

When does the pentose phosphate pathway run?

A

When energy levels are high

289
Q

Why does the pentose phosphate level only run when energy levels are high?

A

If glycolysis is running, ATP and NADH levels are high, so there is product inhibition and allosteric inhibition of glycolysis. This causes G-6-P levels to rise, and so can enter pathways it wouldn’t otherwise enter as the enzymes Km is too high- the pentose phosphate pathway

290
Q

Where does the pentose phosphate pathway occur?

A

In the cytoplasm

291
Q

How many stages are there in the pentose phosphate pathway?

A

2

292
Q

What are the two stages in the pentose phosphate pathway?

A
  • Oxidative decarboxylation

- Rearrangement to glycolytic intermediates

293
Q

Give the equation for the oxidative decarboxylation stage of the pentose phosphate pathway

A

Glucose-6-phosphate + NADP + → C 5 + CO 2 + NADPH

294
Q

What enzyme is used in the conversion of G-6-P to C 5 ?

A

Glucose-6-P dehydrogenase

295
Q

Give the equation for the arrangement to glycolytic intermediates step in the pentose phosphate pathway

A

3C 5 -sugars → 2 fructose-6-P + glyceraldehyde-3-P

296
Q

What can happen to glyceraldehyde-3-P?

A

It can go back into glycolysis

297
Q

Is the pentose phosphate reversible or irreversible?

A

Irreversible

298
Q

Why is the pentose phosphate pathway irreversible?

A

Because CO 2 is lost

299
Q

What is the pentose phosphate pathway controlled by?

A

NADP + /NADPH ratio

300
Q

How is the pentose phosphate pathway controlled by theNADP + /NADPH ratio?

A

IfNADP + /NADPH ratio high, less NADPH substrate for pathway to run

301
Q

What are the functions of the pentose phosphate pathway?

A
  • Produce NADPH in cytoplasm

- Produce C 5 sugars

302
Q

What is NADPH in the cytoplasm needed for?

A

NAME?

303
Q

Give in example of where biosynthetic reducing power is needed

A

Lipid synthesis

304
Q

Where is there a high level of lipid synthesis

A

In liver and adipose tissue

305
Q

What does the maintenance of free -SH groups on certain proteins prevent?

A

Oxidation to -S-S- (disulphide) bonds

306
Q

What are C 5 sugars needed for?

A

Nucleic acid synthesis

307
Q

What tissues have high levels of nucleic acid synthesis?

A

Ones that divide a lot, e.g. bone marrow

308
Q

What is the result of a G-6-P dehydrogenase deficiency?

A

Means that G-6-P can’t be converted into 5 sugar phosphate, therefore no pentose phosphate pathway and no NADPH produced by this pathway

309
Q

Is G6PDH deficiency common or rare?

A

Common

310
Q

What is the result of G6PDH deficiency in RBCs?

A

The decreased NADPH results in disulphide bonds being formed , which means that haemoglobin is not kept in the reduced form, leading to aggregated proteins called Heinz bodies, which leads to haemolysis, causing anaemia

311
Q

What is the effect of G6PDH deficiency in the lens of eye?

A

Get clouding due to inappropriate disulphide bond formation

312
Q

What must happen to pyruvate at the end of stage 2 of respiration?

A

It must be acted on my pyruvate dehydrogenase

313
Q

What is added to pyruvate when it’s acted upon by pyruvate dehydrogenase?

A

CoA

314
Q

Give the equation for the reaction between pyruvate and CoA

A

Pyruvate + CoA + NAD + → acetyl CoA + NADH + H +

315
Q

What is CoA?

A

A molecule that, when bonded to another molecule, puts in a reactive bond, therefore activating it

316
Q

Where is PDH found in the cell?

A

In the mitochondria

317
Q

Where does the PDH reaction occur?

A

In the mitochondrial matrix

318
Q

How is pyruvate bought into the mitochondrial matrix?

A

Transported across mitochondrial membrane on a protein

319
Q

Why does pyruvate need to be transported into the mitochondrial matrix on a protein?

A

Because it is hydrophilic

320
Q

How many enzymes are in the PDH complex?

A

5

321
Q

How is the PDH complex arranged

A

Neatly, so that substrates and products are passed around the complex

322
Q

What do different enzyme activities require?

A

Various cofactors

323
Q

Give 4 cofactors that enzymes in the PDH complex requires

A

NAME?

324
Q

What provide the cofactors that the PDH complex requires?

A

B vitamins

325
Q

What is the result of B vitamins providing the cofactors required for the PDH complex?

A

The reaction is sensitive to B1 deficiency

326
Q

Is the PDH reaction reversible or irreversible?

A

Irreversible

327
Q

Why is the PDH reaction irreversible?

A

Because it produces CO 2

328
Q

What is the result of the PDH reaction being irreversible?

A

It is a key regulatory step

329
Q

Can pyruvate be formed from acetyl-CoA?

A

No

330
Q

What is the PDH reaction activated by?

A

NAME?

331
Q

Give 5 low energy signals that activate the PDH reaction

A

NAME?

332
Q

What is the PDH reaction inhibited by?

A
  • High energy signals

- Phosphorylation

333
Q

Give 4 high energy signals that inhibit the PDH reaction

A

NAME?

334
Q

What does a PDH deficiency result in?

A

Lactic acidosis

335
Q

How does PDH deficiency cause lactic acidosis?

A

If the PDH reaction goes wrong, can’t pass substrate into the TCA cycle, so pyruvate builds up, which is then converted into lactic acid by lactate dehydrogenase, which causes lactic acidosis

336
Q

Where does the TCA cycle occur?

A

In the mitochondria

337
Q

Is the TCA cycle a single pathway, or multiple pathways?

A

A single pathway

338
Q

What is converted into what in the TCA cycle?

A

Acetyl (CH 3 CO - ) to 2CO 2

339
Q

Is the TCA cycle oxidative or reductive?

A

Oxidative

340
Q

What does the TCA cycle require as it is oxidative?

A

NAD + and FAD

341
Q

Is energy produced in the TCA cycle?

A

Some, in the form of ATP and GTP

342
Q

How is ATP and GTP produced in the TCA cycle?

A

Substrate level phosphorylation

343
Q

Other than energy, what else does the TCA cycle produce?

A

Precursors for biosynthesis

344
Q

What are the key steps in the Krebs cycle?

A

The oxidative steps, where substrate level phosphorylation occurs, and where CO 2 is released

345
Q

What has happened to all the reducing power on the original glucose molecule by the end of the TCA cycle?

A

It has been captured

346
Q

How is the reducing power of glucose captured in the TCA cycle?

A
  • Substrate level phosphorylation

- On reducing carriers

347
Q

What is the overall equation for the TCA cycle?

A

CH 3 CO~CoA + 3NAD + + FAD + GDP + Pi + 2 H 2 O → 2CO 2 + CoA + 3NADH +FADH 2 + GTP

348
Q

What is the overall yield per mole of glucose from the TCA cycle?

A

6 NADH
2 FADH 2
2 GTP

349
Q

How is the TCA cycle regulated?

A
  • By energy availability

- By irreversible steps

350
Q

What ratios regulate the TCA cycle by energy availability?

A
  • ATP/ADP

- NADPH/NADP +

351
Q

What steps in the TCA cycle are irreversible?

A

Ones where CO 2 is removed

352
Q

In what reactions in the TCA cycle is CO 2 removed?

A
  • Isocitrate + NAD + → α-ketoglutarate (C5) + CO 2 + NADH
  • CoA +α-ketoglutarate (C5) +NAD + → succinyl-CoA (C4) +CO 2 + NADH
353
Q

What is the enzyme for the conversion of isocitrate toα-ketoglutarate?

A

Isocitrate dehydrogenase

354
Q

What is isocitrate dehydrogenase regulated by?

A
  • Positively regulated by ADP

- Negatively regulated by ATP and NADH

355
Q

What is the result of isocitrate dehydrogenase being stimulated by ADP?

A

If energy levels are low, then it’s stimulated into activity

356
Q

What is the enzyme of the conversion ofα-ketoglutarate to succinyl-CoA?

A

α-ketoglutarate dehydrogenase

357
Q

What isα-ketoglutarate dehydrogenase inhibited by?

A

It’s product, NADH, and ATP

358
Q

What 5 intermediates in the TCA cycle supply biosynthetic processes?

A

NAME?

359
Q

What biosynthetic processes does citrate supply?

A

Production of fatty acids

360
Q

What biosynthetic processes doesα-ketoglutarate supply?

A

Production of amino acids

361
Q

What biosynthetic processes does succinate supply?

A
  • Production of amino acids

- Production of haem

362
Q

What biosynthetic processes does malate supply?

A

Production of amino acids

363
Q

What biosynthetic processes does oxaloacetate supply?

A

NAME?

364
Q

What is meant by the TCA being a hub?

A

It’s possible to feed in and out of pathway, and convert one thing into another

365
Q

What is TCA in a central pathway in?

A

The catabolism of sugars, fatty acids, ketone bodies, amino acids and alcohol

366
Q

What strategy does the TCA cycle use?

A

Produce molecules that readily lose CO 2

367
Q

What bond is broken in the TCA cycle?

A

The C-C bond in acetate (acetyl~CoA)

368
Q

What are carbons oxidised to in the TCA cycle?

A

CO 2

369
Q

How many oxidative steps are there in the TCA cycle?

A

4

370
Q

What do the oxidative steps in the TCA use?

A

3 using NAD + , 1 using FAD

371
Q

Does the TCA cycle function in the absence of oxygen?

A

No

372
Q

Why does the TCA cycle not function in the absence of oxygen?

A

NADH and FADH 2 being stripped off requires oxidative phosphorylation in mitochondria to be running. If there is no oxygen, there is a build up, so the cycle will stop

373
Q

What happens when the TCA cycle can’t run due to lack of oxygen?

A

We must rely on the energy from glycolysis and lactate dehydrogenase

374
Q

How do the intermediates of the TCA cycle act?

A

Catalytically

375
Q

Why is it said that intermediates in the TCA act catalytically?

A

There is no net synthesis or degradation of the intermediates alone (unless if fed in from other substrates)

376
Q

How much energy does substrate level phosphorylation release?

A

~124kJmol -1

377
Q

Where is the remaining energy to be accounted for in a glucose molecule?

A

In the chemical bonds of NADH and FADH 2

378
Q

How is the energy in NADH and FADH 2 released?

A

High energy electrons are transferred to oxygen, releasing large amounts of energy

379
Q

What is the energy released from NADH and FADH 2 used to do?

A

Drive ATP synthesis

380
Q

Where does stage 4 of catabolism occur?

A

In the mitochondria

381
Q

What happens in stage 4 of catabolism?

A

Electron transport and ATP synthesis

382
Q

What happens to NADH and FADH 2 in stage 4 of catabolism?

A

They’re reoxidised

383
Q

What is the purpose of the reoxidation of NADH and FADH 2 in catabolism?

A

It uses the bond energy released to produce ATP

384
Q

Why is O 2 required in stage 4 of catabolism?

A

It picks up electrons released from reduced carriers

385
Q

What happens to oxygen in stage 4 of catabolism?

A

It is reduced to H 2 O

386
Q

Is ATP produced in stage 4 of catabolism?

A

Yes, large amounts

387
Q

What processes occur in stage 4 of catabolism?

A

NAME?

388
Q

What happens in electron transport?

A

Electrons on NADH AND FADH 2 are transferred through series of carrier molecules to oxygen

389
Q

What is the purpose of electron transport?

A

It releases energy in steps

390
Q

Why does electron transport release energy in steps?

A

It allows control of the process, so the most can be got out of it

391
Q

What happens in oxidative phosphorylation?

A

Free energy is used to drive ATP synthesis

392
Q

Describe the structure of a mitochondrion?

A
  • Have outer membrane and inner membrane, folded into cristae
  • Between membranes is intermembrane space
  • Inside membranes is matrix
393
Q

Are the mitochondrial membranes permeable?

A
  • The outer membrane is quite leaky

- The inner membrane is very impermeable

394
Q

What is the inner membrane especially impermeable too?

A

Hydrogen ions

395
Q

What does the inner mitochondrial membrane contain?

A

All machinery for electron transport

396
Q

What is the significance of proton translocating complexes (PTC) in electron transport?

A

In a number of steps, electrons are passed between electron transport complexes, with a bit of energy being given up each time

397
Q

What happens at proton translocating complex (PTC) 1 in electron transport?

A

NADH gives up an electron to electron transport

398
Q

Give the equation for what happens at PTC 1

A

NADH + H + → NAD +

399
Q

What happens in the mitochondrial membrane once NADH has given up it’s electrons at PTC 1?

A

2e - pass down as energy level in inner mitochondrial membrane, and 2 H + are pushed out to inter membrane space

400
Q

What happens at PTC 2?

A

FAD feeds in

401
Q

Why does FAD have a lower energy yield?

A

Because it feeds in halfway down transport chain, so only get 4 H + ions out of inter membrane space

402
Q

What happens at PTC 3?

A

2 H + are fed in from matrix, 2e - move down and 2 H + are pushed out

403
Q

What happens at the end of the electron transport chain?

A

2H + + O combine with the 2 e - from the inner mitochondrial membrane, on the mitochondrial matrix, forming water

404
Q

What are electrons transferred through in the electron transport chain?

A

A series of carrier molecules

405
Q

Where are the carrier molecules electrons are transferred through mostly found?

A

Within proteins

406
Q

How much of the energy is used to move H + across the membrane?

A

~30%

407
Q

How is a lot of energy lost in the electron transport chain?

A

As heat

408
Q

Why is it important that some energy is lost as heat in the ETC?

A

To maintain body heat

409
Q

What is meant by membrane potential?

A

The [H + ] gradient across the inner membrane of mitochondria

410
Q

What does the membrane potential create?

A

Proton motive force

411
Q

How is the proton motive force induced?

A

Every time you transfer positive ion out of the matrix, negative anion must be left behind, generating an electrical potential across the membrane, creating a driving force on hydrogen ions that want to come back into matrix

412
Q

What gradients are now supporting hydrogen ions wanting to come back into the matrix?

A

NAME?

413
Q

What does the proton motive force create?

A

Stored up potential energy

414
Q

Give the reaction that proton translocating ATPase catalyses

A

ATP + 2H + (mitochondrial matrix) ↔ ADP + Pi + 2H + (cytoplasm)

415
Q

What is the energy released by proton translocating ATPase used to do?

A

Drive H ions out into the inner membrane space

416
Q

Is the proton translocating ATPase reaction reversible or irreversible?

A

Reversible

417
Q

What is the result of the proton translocating ATPase reaction being reversible?

A

The gradient of H ions set up by electron transport can be used, if we allow H ions to run back into the matrix down their electrochemical gradient, releasing energy

418
Q

What can the energy released when hydrogen ions come back in through proton translocating ATPase be used for?

A

To drive synthesis of ATP

419
Q

Why is the proton gradient created effectively doing oxidative phosphorylation?

A

Because the products of oxidation are driving the phosphorylation of ATP from ADP using the proton gradient between two mitochondrial membranes, as the return is highly energetically favourable

420
Q

What is energetically favoured by the electrochemical potential?

A

Return of protons across the membrane, from the inner mitochondrial space to the matrix

421
Q

What is the only way protons can return across the membrane to the matrix?

A

Via the ATP synthase

422
Q

Why can protons only return across the membrane through ATP synthase?

A

Due to the impermeability of the inner mitochondrial membrane

423
Q

What is the result of protons only being able to return through ATP synthase?

A

It drives ATP synthesis

424
Q

What is ATP synthesis coupled to?

A

Electron transport

425
Q

How is electron transport coupled to ATP synthesis?

A

Electrons are transferred from NADH and FADH 2 to molecular oxygen, releasing energy to generate the p.m.f. Energy from the dissipation of p.m.f. is coupled to synthesis of ATP from ADP, further capturing the energy

426
Q

How many PTC’s does NADH use?

A

3

427
Q

How many PTC’s does FADH 2 use?

A

2

428
Q

Why does NADH use more PTCs than FADH 2 ?

A

Because electrons in NADH have more energy

429
Q

What is the result on p.m.f. of NADH having more energy than FADH 2 ?

A

More p.m.f. from NADH

430
Q

What does a greater p.m.f. mean for ATP synthesis?

A

More ATP synthesised

431
Q

How is oxidative phosphorylation regulated by ADP?

A

When [ADP] decreases, no substrate for ATP synthesis, so the inward flow of H + stops. This leads to an increase in [H + ] in the intermitochondrial space, which prevents furtherH + pumping, stopping electron transport. As electron transport and oxidative phosphorylation are tightly coupled, this inhibits both

432
Q

Give an example of an inhibitor of electron transport (other than ADP)

A

Cyanide

433
Q

How do inhibitors such as cyanide block electron transport?

A

By preventing acceptance of electrons by oxygen

434
Q

What happens when an inhibitor blocks the acceptance of electrons by oxygen?

A

The flow of electrons ceases, which means there is no p.m.f. and therefore no oxidative phosphorylation

435
Q

What structures are electron carriers similar to?

A

That of haem

436
Q

What is the result of electron carriers using a similar structure to that of haem?

A

CO can inhibit

437
Q

Why can CO inhibit electron carriers?

A

It binds with a higher affinity that oxygen

438
Q

What affect does cyanide have on electron transport?

A

It blocks electron acceptance by oxygen, therefore causing a build up of electrons, so no energy is given up to put H + in inner membrane space, and so decreasing the p.m.f. and consequently ATP.

439
Q

What do uncouplers do?

A

Increase the permeability of mitochondrial inner membrane to protons

440
Q

What is the result of the increased permeability of the inner membrane to protons?

A

Won’t have to go through ATP synthase

441
Q

What happens to the p.m.f. because of uncouplers?

A

Reduces it

442
Q

Why do uncouplers reduce the p.m.f.?

A

Because it dissipates the proton gradient

443
Q

In the presence of uncouplers, what happens to the energy instead of it driving ATP synthesis?

A

It is released as heat instead

444
Q

Does electron transport continue when uncoupling has occurred?

A

Yes

445
Q

Why does electron transport continue even after uncoupling?

A

Because there is no inhibition

446
Q

Give 3 examples of things that can act as uncouplers

A

NAME?

447
Q

What are ox/phos diseases?

A

Generic defects in proteins encoded by mtDNA

448
Q

What proteins encoded for by mtDNA are defective in ox/phos diseases?

A

Some sub-units of the PTC and ATP synthase

449
Q

What is the result of the defective proteins in ox/phos diseases?

A

Decreased electron transport and ATP synthesis

450
Q

What is the result of inefficiency in coupling?

A

Energy lost as heat

451
Q

What does efficiency of coupling depend on?

A

Tightness of coupling

452
Q

Where can the tightness of coupling be varied?

A

Brown adipose tissue

453
Q

What is the degree of coupling controlled by in brown adipose tissue?

A

Fatty acids

454
Q

What does the control of coupling in brown adipose tissue allow for?

A

Extra heat generation

455
Q

What does brown adipose tissue contain?

A

Thermogenin (UCP1)

456
Q

What is UCP1?

A

A naturally occurring uncoupling protein

457
Q

What happens in response to cold?

A

Noradrenaline activates lipase and fatty acid oxidation

458
Q

What is the affect of lipase oxidation?

A

It released fatty acids from triacylglycerol

459
Q

What does fatty acid oxidation produce?

A

NADH and FADH 2

460
Q

What happens to the NADH and FADH 2 released by fatty acid oxidation?

A

They go into electron transport

461
Q

What do fatty acids activate?

A

UCP1

462
Q

What does UCP1 do?

A

Transports H + back into the mitochondria

463
Q

What happens when UCP1 transports H + back into the mitochondria?

A

NAME?

464
Q

Where is brown adipose tissue found?

A

NAME?

465
Q

Why is brown adipose tissue found in newborn infants?

A

To maintain heat, particularly around vital organs

466
Q

Why is the extra heat from brown adipose tissue needed in newborn infants?

A

Because they have a small SA to volume ratio

467
Q

What is the difference in requirements for oxidative and substrate level phosphorylation?

A
  • Oxidative requires membrane-assoicated complexes

- Substrate level requires soluble enzymes

468
Q

What is the difference between methods of energy production in oxidative and substrate level phosphorylation?

A
  • In oxidative, energy coupling occurs indirectly through the generation and subsequent utilisation of a proton gradient
  • In substrate level, energy coupling occurs directly, through formation of high energy hydrolysis bond (phosphoryl-group transfer)
469
Q

What is the difference in oxygen requirement between oxidative and substrate level phosphorylation?

A

NAME?

470
Q

What is the difference in significance of amount of ATP produced between oxidative and substrate level phosphorylation?

A
  • Oxidative is major ATP synthesis process in cells

- Substrate level is minor process for ATP synthesis

471
Q

When is substrate level phosphorylation the major process for ATP synthesis?

A

NAME?

Z OLD ESA 1- Metabolism (17 decks)

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