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Flashcards in Biology Class 2 Deck (24)
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1

Catabolism vs Anabolism

Breaking down vs Building up

2

Oxidation vs Reduction

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

3

Process, Location & O2 requirement

Glycolysis, cytosol, no O2

PDC/ Krebs Cycle, mitochondrial matrix, needs O2

ETC/Oxidative Phosphorylation, inner mitochondrial matrix, needs O2

4

Goal of ETC

1. oxidize (empty) e- carriers
2. make usable energy (ATP)

5

Process of ETC

- 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

6

How much energy is 1 NADH and 1 FADH2?

2.5 and 1.5 respectively

7

What if there is no O2 in ETC?

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

8

How do you allow glycolysis to happen without O2?

For 1 pyruvate (glycolysis makes 2):
- reduce it to ethanol (yeast) & lactic acid (muscles) by oxidizing NADH produced back to NAD+

9

Problems with proceeding with glycolysis with no O2?

- end products are toxic
- only make 2 ATP per glucose vs 30 (not enough to survive)

10

Reciprocal Regulation

Same molecule regulates 2 enzymes in opposite ways
Eg. Citrate inhbits PFK -> inhibits glycolysis BUT activates Fruc 1,6 bis Pase -> activates gluconeogenesis

11

Role of Fruc-2,6-bisP

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

12

Glycogenesis vs Glycogenolysis

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

13

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

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

14

What does the Pentose Phosphate pathway achieve?

Produces 2 NADPH & ribose 5-phosphate

15

NADPH

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

16

Ribose 5-phoshpate

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

17

FA Metabolism

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

18

FA Oxidation (FA breakdown)

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)

19

How to make malonyl Co-A?

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

20

FA Synthesis - Activation & Elongation

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

21

Ketogenesis

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

22

Ketone Body Formation

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

23

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

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

24

Protein Catabolism

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