Biology Class 2

Question 1

Catabolism vs Anabolism

Answer 1

Breaking down vs Building up

Question 2

Oxidation vs Reduction

Answer 2

Oxidation - loss of e-, loss of H+, gain of O

Reduction - gain of e-, gain of H+, gain of O

Question 3

Process, Location & O2 requirement

Answer 3

Glycolysis, cytosol, no O2

PDC/ Krebs Cycle, mitochondrial matrix, needs O2

ETC/Oxidative Phosphorylation, inner mitochondrial matrix, needs O2

Question 4

Goal of ETC

Answer 4

1. oxidize (empty) e- carriers

2. make usable energy (ATP)

Question 5

Process of ETC

Answer 5

• Taking e- through its carriers to the last e- carrier which is O2 and it will then be reduced to H2O
• The more NADH that is put into the system, the more e-, therefore the more H+ protons being pumped against the gradient through ATP synthase to allow ADP to phosphorylate to ATP

Question 6

How much energy is 1 NADH and 1 FADH2?

Answer 6

2.5 and 1.5 respectively

Question 7

What if there is no O2 in ETC?

Answer 7

E- will not go through carriers so you will accumulate NADH and have a decrease in NAD+ and FAD

Question 8

How do you allow glycolysis to happen without O2?

Answer 8

For 1 pyruvate (glycolysis makes 2):

- reduce it to ethanol (yeast) & lactic acid (muscles) by oxidizing NADH produced back to NAD+

Question 9

Problems with proceeding with glycolysis with no O2?

Answer 9

• end products are toxic

- only make 2 ATP per glucose vs 30 (not enough to survive)

Question 10

Reciprocal Regulation

Answer 10

Same molecule regulates 2 enzymes in opposite ways

Eg. Citrate inhbits PFK -> inhibits glycolysis BUT activates Fruc 1,6 bis Pase -> activates gluconeogenesis

Question 11

Role of Fruc-2,6-bisP

Answer 11

Signals abundance of glucose, therefore:
- high glucose -> activates insulin -> activates fruc-2,6-bisP -> activate glycolysis to break down glucose molecules to ATP

• low glucose -> activates glucagon -> inhibits fruc-2,6-bisP -> activates gluconeogenesis to make glucose

Question 12

Glycogenesis vs Glycogenolysis

Answer 12

Glycogenesis

• synthesize glycogen because high blood sugar
• Hormone produced: insulin
• Glucose is converted to glycogen and is stored in liver and to a lesser extent in skeletal muscle

Glycogenolysis

• breakdown glycogen to glucose because low blood sugar
• Hormones produced: glucagon & adrenaline

Question 13

Why do you tap into liver and not skeletal muscle for glucose?

Answer 13

Need glucose 6-P to make glucose and phosphate is negatively charged & cannot cross the skeletal muscle membrane

Question 14

What does the Pentose Phosphate pathway achieve?

Answer 14

Produces 2 NADPH & ribose 5-phosphate

Question 15

NADPH

Answer 15

• reducing power for anabolic rxs
• eliminates free radicals, protects cell from DNA, membrane & other damage
• is an e- carrier

Question 16

Ribose 5-phoshpate

Answer 16

• nucleotide synthesis (if a cell is dividing, it needs this ribose 5-phosphate)

Question 17

FA Metabolism

Answer 17

Release of FA
- triglyceride (1 glycerol + 3 FAs) + lipase will break it down to individual components

Conversion to acyl Co-A

• FA in presence of ATP will react with CoA and make 6 carbon aceylCoA in the cytosol
• will travel to matrix and enter b-oxidation where it will go through 2 rounds (first releasing 1 acetylCoA, then 2, total of 3)
• then will enter Kreb’s Cycle

Question 18

FA Oxidation (FA breakdown)

Answer 18

Saturated Fat

• 6C acyl CoA which will be oxidized to introduce double bond by converting FAD to FADH2
• further oxidize to intro carbonyl so will convert NAD+ to NADH
• break it into a 2C acetylCoA through B-oxidation, and 4C (Which will subsequently break into 2 acetylCoA by feeding back into B-oxidation)

Unsaturated Fat

• 6C acyl CoA (where double bond may be in wrong place so may have to rearrange
• oxidize to intro carbonyl so will convert NAD+ to NADH
• break it into a 2C acetylCoA through B-oxidation, and 4C (Which will subsequently break into 2 acetylCoA by feeding back into B-oxidation)

Question 19

How to make malonyl Co-A?

Answer 19

Acetyl CoA (2C) + bicarb (HCO3-) in presence of ATP will make Malonyl CoA (3C)

Question 20

FA Synthesis - Activation & Elongation

Answer 20

Activation

Acetyl CoA + acyl carrier protein (ACP) -> Acetyl-ACP + CoA -> Acetyl Fatty acide synthase (Acetyl FAS)

Malonyl CoA + ACP -> Malonyl-ACP + CoaA

At the end stages of both, it’ll be active & react with each other

Elongation

• Both react (5C) but lose 1 C through CO2
• Forms 4C-ACP
• Then have NADPH from PPP which is reduced to NADP+
• Still have 4C-ACP
• Then further reduce another NADPH from PPP to NADP+
• Form 4C-FAS which goes back to the cycle
• 4C-ACP goes from ACP binding site 1 to binding site 2 FAS
• 4C FAS is now active but ACP binding site is empty so malonyl-CoA (3C) will bind at ACP
• the 2 react and you lose 1 C and end up with 6 C which will enter the cycle again etc

Question 21

Ketogenesis

Answer 21

Where acetyl Co-A react together to form ketone bodies

• During long term starvation, blood glucose levels fall
• To meet energy demand, FAs are oxidized to form acetyl CoA
• Levels of acetyl-CoA increase; some feed into Krebs Cycle while some react togehter to enter brain
• Ketone bodies can pass through blood-brain barrier and be reconverted to acetyl CoA during starvation

Question 22

Ketone Body Formation

Answer 22

acetyl CoA + acetyl CoA = acetoacetate –> hydroxybutyrate + acetone (all 3 are ketone bodies)

Question 23

How can having too many ketone bodies result in suffering from ketoacidosis?

Answer 23

Ketone bodies have H+ attached to it so it makes it acidic thus blood pH is low. Too many will make it too acidic

Question 24

Protein Catabolism

Answer 24

Proteins from body break down into individual A.A.

• A.A. can be used to make other proteins needed by body OR
• forms amino (which in turn becomes urea which is eliminated via urine or other nitrogenous compounds eg DNA bases)
• forms carbon skeleton (which in turn pyruvate can form glucogenic a.a. or vice versa / acetyl Co-A can form ketogenic a.a. or vice versa