Metabolism 5-6

Question 1

What is the evidence for mitochondria being evolutionarily derived from prokaryotes?

Answer 1

• Has its own genome which resembles a prokaryotic genome
• First amino acid in mitochondrial transcript is formulated methionine (fMet) same as bacteria but eukaryotic is it methionine
• Can synthesise their own proteins
• Not associated with histone proteins which is the same as prokaryotes
• Can only arise from pre-existing mitochondria
• Some antibiotics which target bacterial protein synthesis also inhibit mitochondrial protein synthesis

Question 2

What are the membrane complexes involved in the ETC?

Answer 2

• NADH dehyrodrogenase complex
• Cytochrome b-c1 complex
• Cytochrome oxidase

Question 3

What are the mobile carriers associated with ETC?

Answer 3

• Ubiquinone (Co-enzyme Q)

- Cytochrome C

Question 4

How does the ETC work?

Answer 4

• The proteins accept electrons and in doing so a proton from the aqueous solution is passed across to the inter-membrane space.
• Each unit of the chain has a higher affinity for electrons that the one before making sure that the electrons move in a logical order.

Question 5

What is cytochrome oxidase and what does it do?

Answer 5

Terminal electron acceptor in the ETC. Recieves 2 electrons from cytochrome C mobile carrier but two rounds of this will equal 4 electrons which can be donated to oxygen to form water.

Question 6

What is a redox reaction?

Answer 6

Reaction involving electron transfer between a reduced substrate and oxidised substrate.

Question 7

What is a redox couple?

Answer 7

Substrate that can exist in both oxidised and reduced forms.

Question 8

What is the redox potential?

Answer 8

Ability of a redox couple to accept or donate electrons which can be determined experimentally.

Question 9

What does a negative redox potential indicate?

Answer 9

Tendency to donate electrons.

Question 10

What does a positive redox potential indicate?

Answer 10

Tendency to accept electrons.

Question 11

What is ATP synthase?

Answer 11

Multimeric enzyme consisting of a membrane-bound region (F0 - A, B, C) and a region that project into the matrix space (F1 - a,b,g).

Question 12

How does ATP synthase work?

Answer 12

When protons flow through the membrane via the pore, the c (and attached gamma subunits) rotate, driving structural changes and altering the affinity for ADP AND ATP. The direction of flow of protons determines whether ATP synthesis or hydrolysis will take place.

Question 13

What is the life span of ATP?

Answer 13

1-5 minutes, regenerated 300 times a day.

Question 14

How does malonate work?

Answer 14

Resembles succinate so it can act as a competitive inhibitor for succinate dehydrogenase, slowing down the flow of electrons from succinate to ubiquinone by inhibiting the oxidation of succinate to fumarate.

Question 15

How does rotenone work?

Answer 15

Found in plants and roots. Inhibits the transfer of electrons from NADH dehydrogenase to ubiquinone.

Question 16

When in non-shivering thermogenesis used?

Answer 16

In brown adipose tissue in newborn babies and hibernating animals.

Question 17

How does non-shivering thermogenesis?

Answer 17

• In response to a temperature drop, hormone secretion induces fatty acid liberation from triacylglycerides.
• This activates thermogenin (UCP-1)
• UCP-1 allows protons to bypass ATP synthase to cross over into the matrix space, thereby releasing heat instead of in the form of ATP
• Similar to DNP

Question 18

What are the sources of fat?

Answer 18

• Diet
• De novo biosynthesis (lipogenesis)
• Adipocytes

Question 19

What are bile salts derived from?

Answer 19

Cholesterol

Question 20

Where are bile salts made and stored?

Answer 20

Made in the liver and stored in the gall bladder.

Question 21

What do bile salts do?

Answer 21

Have hydrophilic and hydrophobic regions allowing them to emulsify fats and lipid-soluble vitamins (A, D, E and K) in the small intestine.

Question 22

What does a lack of bile salts result in?

Answer 22

Undigested fats passing through the gut and excreted resulting is steatorrhea (fatty stool)

Question 23

How are digested diary products absorbed?

Answer 23

By enterocytes.

Question 24

What is beta oxidation?

Answer 24

The breaking down of fatty acids (normally palmitic acid) into acetyl-CoA subunits which then enter the Krebs cycle.

Question 25

How many acetyl-CoA subunits can palmitic acid produce?

Answer 25

8

Question 26

When do acetyl-CoA enter the Krebs cycle?

Answer 26

If beta-oxdiation and lipid metabolism are balanced as oxaloacetate is needed for entry.

Question 27

What happens if beta-oxidation predominates?

Answer 27

Acetyl-CoA forms acetoacetate-D-3-hydroxybutyrate and acetone (ketone bodies).

Question 28

Where does beta oxidation occur in a cell?

Answer 28

Mitochondrial matrix

Question 29

What is the reducing power in beta-oxidation?

Answer 29

NADPH

Question 30

What is the reducing power in lipogenesis?

Answer 30

NADH and FAD

Question 31

Where does lipogenesis take place?

Answer 31

Mitochondrial matrix

Question 32

What is the process of lipogenesis?

Answer 32

1) Formation of malonyl-CoA
2) Transfer of malonyl-CoA to ACP to form malonyl-ACP.
3) Same is done for acetyl forming acetyl-ACP.
4) Condensation of the two ACP linked molecules forming 4C fatty acid species
5) Reduction to D-3-hydroxybutyryl-ACP
6) Dehydration to crotonyl-ACP
7) Further catalysed to butyric-ACP.
Repeat steps 4-7 another 6 times to form 16C species (palmitoyl-ACP)

Question 33

What happens in lipogenesis (basically)?

Answer 33

Formation of fatty acids using malonyl-CoA and acetyl-CoA through decarboxylative condensation reactions.

Question 34

What does ACP stand for?

Answer 34

Acyl carrier protein

Question 35

What is the carnitine shuttle used for?

Answer 35

Shuttling acyl-CoA spices into the matrix where beta oxidation takes place.

Question 36

How does the carnitine shuttle work?

Answer 36

• Acyl group his coupled with carnitine to form acyl-carnitine using carnitine acyltranferase.
• Shuttled across the membrane using translocase.

Question 37

What is primary carnitine deficiency?

Answer 37

• Autosomal recessive disorder
• Symptoms develop during infancy or childhood
• Reduced ability to take up carnation which is needed for oxidation of fatty acids
• Encephalopathies, cardiomyopathies, muscle weakness and hypoglycaemia.