S2: Energy II: Acetyl CoA, Mitochondria and Oxygen Flashcards Preview

MCBHD- Molecular and Cellular Basis of Health and Disease > S2: Energy II: Acetyl CoA, Mitochondria and Oxygen > Flashcards

Flashcards in S2: Energy II: Acetyl CoA, Mitochondria and Oxygen Deck (28)
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1
Q

What is aerobic respiration?

A

Aerobic respiration occurs only in the presence of O2 and yields more energy in the form of ATP and requires the citric acid cycle and oxidative phosphorylation. It take place in the mitochondria.

2
Q

Explain the structure of mitochondria and where different aspects of respiration occur on them

A

There is an outer mitochondrial membrane and an inner mitochondrial membrane with the intermitochondrial space in between. On the inside there is the matrix.

Matrix - TCA cycle occurs

Inner mitochondrial membrane - Oxidative phosphorylation occurs

3
Q

Describe the citric acid cycle (kreb cycle)

A

Pyruvate undergoes the links reaction to become acetyl CoA. CO2 and NADH is generated in this process.

ACoA enters TCA cycle which and reacts with 4C acid (oxaloacetate) to become a 6C acid (citrate).

Amount of oxaloacetate remains the same it is continually recycled.

Citrate then goes under a series of reaction resulting in loss of 2CO2 becoming a 4C molecule.

4
Q

Net production in TCA cycle

A
Forr each glucose (2 pyruvate):
	• 6 NADH (within)+ 2 
           NADH (In producing ACoA)
	• 2 FADH2
	• 2 GTP
        • 4 CO2 + 2CO2  (in 
           producing ACoA)
5
Q

What is the purpose of TCA cycle?

A

The purpose is to generate the NADH and FADH2 to be used in the ETC thus providing most electrons for oxidative phosphorylation.

TCA also integrates carbohydrate, lipid and protein metabolism as these can enter as ACoA.

6
Q

What regulates entry into the citric acid cycle?

A

The formation of ACoA from pyruvate which uses the enzyme pyruvate dehydrogenase.

7
Q

What regulates pyruvate dehydrogenase?

A

This enzyme is inhibited by NADH and ACoA (products of the link reaction).

The enzyme is also regulated by phosphorylation ATP (covalent modification) which inhibits its activity

This is because build up informs the enzyme that the energy needs of the cell are being met or that fatty acids are being broken down to produce NADH and acetyl CoA - inhibiting pyruvate dehydrogenase spares glucose.

It is stimulated by ADP and pyruvate

8
Q

What happens to excess glucose?

A

Excess glucose –> increased pyruvate –> increased fatty acid synthesis (instead of TCA)

9
Q

Explain ways pyruvate dehydrogenase is activated

A

In muscle –> it is activated via action of phosphatase (which removes phosphorylation). This phosphatase in muscle is stimulated by Ca2+. This allows the muscle to link contraction to a process that will generate ATP.

10
Q

Explain in ways phosphatase is activated

A

Muscle = via Ca2 which activates pyruvate dehydrogenase involved in producing ATP

Liver and adipose tissue= Insulin stimulates the phosphatase which funnels glucose to fatty acid synthesis. This process is for storage rather than producing ATP.

11
Q

State 3 more regulation points within the citric acid cycle

A
  1. The convertion of ACoA –> Citrate under the action of the enzyme citrate synthase.
  2. Isocitrate –> a-ketogluterate by enzyme isocitrate dehydrogenase.
  3. a-ketogluterate –> Succinyl CoA by enzyme a-ketodehydrogenase.
12
Q

What enzyme converts ACoA to Citrate and what regulates it?

A

Citrate synthase

It is inhibited by citrate. This means in cases where there is enough ATP the ACoA will be directed to other routes e.g. fatty acid synthesis

13
Q

What enzyme converts Isocitrate to a-ketogluterate and what regulates it?

A

Isocitrate dehydrogenase

It is inhibited by NADH, ATP, Succinyl CoA

14
Q

What enzyme converts a-ketogluterate to Succinyl CoA and what regulates it?

A

a-ketodehydrogenase

It is inhibited by NADH, ATP and Succinyl CoA

15
Q

What is Beriberi?

A

It is a deficiency in thiamine (vitamin B1).

It is common in far-east where rice is a staple diet.

Thiamine is a prosthetic group for enzymes pyruvate dehydrogenase and a-ketogluterate dehydrogenase. These enzymes are important in regulating the TCA cycle so someone with Beriberi has an inability to generate sufficient ATP.

This disease is therefore characterised by cardiac and neurological symptoms.

16
Q

What is the fate of NADH and FADH2?

A

From TCA they are used in the electron transport chain for oxidative phosphorylation

17
Q

Explain the electron transport chain and ATP synthesis

A

Hydrogen atoms are removed from NADH and FADH2. The hydrogen atoms enter the ETC and each is split to give an electron and proton (oxidation of NADH)

The electron is passed through a series of enzymes called cytochromes from left to right going from high energy to low energy state (this powers proton pumps). It finally reacts with molecular oxygen with H+ to form water.

The proton is pumped across the inner mitochondrial membrane into the intermembrane space to establish a gradient.

H+ diffuse down their gradient through ATP synthase into the matrix. This generates ATP from ADP.

18
Q

What are electron carriers in ETC called?

A

They are enzymes called cytochromes

19
Q

How many protons needed for 1 ATP?

A

3

20
Q

How many protons needed to transport ATP out of matrix?

A

1

21
Q

How many ATP do we get from every NADH and FADH2?

A

For every NADH we get 3 ATP

For every FADH2 we get 2 ATP (misses one proton complex)

22
Q

Describe ATP synthase

A
  • Transmembrane protein

- Acts as a motor (bottom parts rotates)

23
Q

How many H+ are pumped into intermembrane space for every NADH and FADH2?

A

10 H+ are pumped out for every NADH

6 H+ are pumped out for every FADH2

24
Q

Explain incidences where proton movement across inner mitochondrial membrane is not coupled with ATP synthesis

A

Neonates posses brown fat.

Some of the mitochondria in an infant are different to adult. One difference is they contain a protein called uncoupling protein, which uncouples the proton gradient with ATP synthesis.
Uncoupling protein is an alternative route by which H+ can move down its conc. gradient and in doing so it doesn’t generate ATP it generates heat.

25
Q

Why do neonates posses brown fat?

A

Neonates do not have the ability to shiver and obviously shivering is a good way of generating heat, so a newborn who cannot generate heat will lose heat from their surface.

26
Q

What is brown fat?

A

It is fat that contains a large number of mitochondria (containing coloured cytochromes) giving the brown fat its colour

In neonates is is found predominantly around the neck and shoulders

27
Q

What is OPHOS disease?

A

Group of diseases that are degenerative and caused by mutations in genes encoding proteins of the ETC.
They lead to a number of symptoms including fatigue, epilepsy and dementia.
Depending on the mutations, symptoms may be evident near birth the early adulthood.

A metabolic consequence can be congential lactic acid

28
Q

What regulates ETC?

A
  • It is governed by the cells need for ATP
  • Electron transport is tightly coupled to the demands of the cell for energy (tightly coupled to phosphorylation i.e. ADP -> ATP)
    There are exceptions -> Regulated uncoupling (in tissue where uncoupling protein is expressed) leads to generation of heat