The Krebs cycle

Question 1

What is the krebs cycle?

Answer 1

Continuation of glycolysis to release more ATP from the oxidation of carbon to CO2

Question 2

Where does the krebs cycle occur?

Answer 2

inner membrane of Mitochondria - matrix

Question 3

What are the starting products for the krebs cycle?

Answer 3

Actyle-CoA

Oxaloacetate

Question 4

What needs to be present for the krebs cycle to occur?

Answer 4

Oxygen

Question 5

Which substrates from which molecules can feed into the krebs cycle?

Answer 5

Glucose
Fatty acids
amino acids

Question 6

How is acetyle CoA formed?

Answer 6

Pyruvate is oxidised to produce Acetyle CO-A
Enzyme- pyruvate dehydrogenase complex
NAD+ is reduced to NADH

Question 7

Is acetyle CoA formation reversible? And why?

Answer 7

No

CO2 is lost

Question 8

Which vitamin is important for the TCA cycle and why?

Answer 8

Vitamine B

All enzymes and Co-enzymes involved in acetyle co A formation are made from Vitamin B

Question 9

How is pyruvate dehydrogenase controlled?

Answer 9

2 ways:
1. Allosterically- inhibited by products (Acetyle CO-A and NADH) negtaive feedback

2. By kinase and phosphate enzymes.
   Kinases- inhibit PDC by adding PO4
   Phosphates- activate PDC by removing PO4

Question 10

What is the basic process in TCA cycle

Answer 10

Acetyle CO-A —–oxaloacetete—-Citric acid—-oxaloacetete

Question 11

What are the end products of the TCA cycle?

Answer 11

1 GTP/ATP
3 NADH ( 2ATP each)
1 FADH (2ATP each)

Question 12

What is the mechanism of the electron transport chain?

Answer 12

Electrons from NADH AND FADH used to create a proton gradient across inner membrane of mitochondria

Electrons are transferred down an energy gradient to allow H+ to be pumped out of the membrane

Question 13

What are the ETC complexes? Describe each one

Answer 13

Enzymes found in the inner membrane of the mitochondria
Complex 1- oxidises NADH to NAD+ and 2e-. Transfers electrons to ubiquinone
Complex 2- FADH-FAD+ transferes electrons to ubiquinone
Complex 3- Transfers electrons from ubiquinone to cytochrome C
Complex 4: transfers electrons from cytochrome C to to oxygen to produce water
Energy released at each stage pumps protons from the matrix into the outermembrane

ATP is generated when the protons are allowed back into the matrix through the ATP synthase enzyme.
(oxidative phosphorylation)

Question 14

What is coupling in the TCA cycle?

Answer 14

When electrons are transferred from NADH/FADH down energy states using oxidative reactions whilst protons are being moved outside the membrane binding the electrons with water

Question 15

What is uncoupling in the TCA cycle? How is this used in children?

Answer 15

proton gradient doesnt produce ATP
Non-shivering thermogenesis- Produces heat instead of ATP. uses the uncoupling protein theremogenin found in brown adipose tissue (occurs in infants)

Question 16

Examples of uncouplers

Answer 16

Dinitrophenol (DNP) Disrupts interacation between ETC and proton pump. Protein gradient does not generate ATP

Cyanide- blocks cytochrome and uncouples ATP production

Question 17

How is the TCA cycle controlled?

Answer 17

ATP/NADH inhibition. Negative feed back inhibits 2 dehydrogenase enzymes
Calcium in skeletal muscles activates the dehydrogenase enzymes to produce ATP

No oxaloacetet, NAD+ or Acetyl-CoA? No reaction

Question 18

What else can the krebs cycle generate?

Answer 18

Fatty acids

Glucose

Question 19

What are reactive oxygen species? How are they formed?

Answer 19

high energy molecules that can disrupt of the molecules and result in damage to lipids, proteins and DNA.

electrons are not transported efficiently in TCA cycle

Question 20

What is hypoxia? How does it lead to more ROS production?

Answer 20

a condition of low oxygen concentration.

Hypoxia causes the production of even more ROS since oxygen is not there to mop up electrons.

Question 21

How do cells adapt in a hypoxic enviroment? How are these adaptions obtained?

Answer 21

Limits the amount of ATP needed (since it cannot produce ATP my the ETC)
Improve anaerobic ATP prudction efficiency
Limit oxidative stress (ROS) to prevent damage to tissues

Most of this is achieved by the increased expression of hypoxia –induced factor -1 (HIF1) gene and protein.

Question 22

What is the function of the hypoxia –induced factor -1 (HIF1) gene?

Answer 22

Reduction in mitochondria by promoting their degradation (autophagy)
Inhibits the synthesis of new mitochondria by blocking PGC1 activity.

Question 23

How is HIF1 an oncogene?

Answer 23

Because it allows tumours them to survive in low oxygen due to lack of blood supply