EXAM3_L31_TCA_ETC_OXPHOS

Question 1

What are the 5 coenzymes of PDHC?

TFNCL (thursday,friday, night comes laughter)

Answer 1

Tpp-B1- Thiamine
Fad-B2- riboflavin
Nad-B3- niacin
Coa-B5- PAN TO THE NATE (pantothenate)
LipoicAcid

Question 2

What products come from 1 acetyl CoA?

Answer 2

3 NADH
2 CO2
1 FADH2
1 GTP

Question 3

What happens to TCA if no oxygen?

Answer 3

Buildup of NADH, FADH2 (b/c decreased ETC)

buildup NADH will inhibit TCA (PDHC)

Question 4

Glucose cannot be formed (de novo) by using what from the TCA?

Answer 4

Glucose can’t be made from Acetyl CoA from TCA

Question 5

All regulatory enzymes in TCA are located in the Mitochondrial matrix except?

Answer 5

Succinate Dehydrogenase (inner mitochondrial membrane)
- part of Complex II of ETC

Question 6

What are the 4 Regulatory Enzymes of TCA?

Which one is rate limiting enzyme?

Answer 6

1. Citrate Synthase
2. ICDH* (rate limiting)
3. a-KGDHC
4. Succinyl CoA Synthesis (SS)

Question 7

The rate limiting enzyme ICDH is activated and inhibited by?

Answer 7

Activated by ADP

Inhibited by NADH and ATP

Question 8

What TCA enzyme requires the same 5 coenzymes as PDHC?

Answer 8

Alpha ketogluterate dehydrogenase

TFNCL

Question 9

ADP : ATP ratio is fixed so if you have too much ADP?

What does ADP activate?

Answer 9

you don’t have enough ATP

ADP activates ICDH

Question 10

TCA Cycle is NOT regulated by Insulin, Glucagon, Epinephrine and is ALWAYS ON, so what regulates it?

Answer 10

energy levels of (ATP, NADH, ADP)

and [intermediates] mainly OAA levels

Question 11

Where is OAA derived? What enzyme required?

Answer 11

Pyruvate is converted to OAA by pyruvate carboxylase

Question 12

How is TCA primed?

Answer 12

Pyruvate is converted to OAA by pyruvate carboxylase to start the cycle

Question 13

What are the levels of NADH and ATP in the Fasted State?

Answer 13

High NADH and HIGH ATP (beta oxidation used)

- TCA inhibited and slows down

Question 14

Where does NADH and ATP come from when fasting?

Why is TCA inhibited during fasting?

Answer 14

Beta oxidation makes NADH & FADH2 > ATP

the High levels of NADH inhibit the TCA

Question 15

When citrate accumulates in TCA (fed state) what happens to it?

Answer 15

Exported to cytosol via Citrate Shuttle to deliver Acetyl-CoA

FATTY ACID SYNTHESIS then occurs

(acetyl coa can’t exit tca by itself, has to be in citrate form)

Question 16

What TCA intermediate used for heme synthesis?

Answer 16

Succinyl-CoA

Question 17

OAA can’t exit TCA into cytosol (fasted state) by itself so it uses what shuttle to get into cytosol?
What is it then used for?

Answer 17

Malate Shuttle to be used in gluconeogenesis

-malate carries OAA to the cytosol in the fasted state

Question 18

What three areas is Thiamine essential for?

Answer 18

1. PDHC
2. alpha-KGDH (TCA)
3. branch chain ketoacid dehydrogenase (muscle/brian energy)

Question 19

What is beri-beri?

Answer 19

Thiamine (Vit B1) deficiency “weak! weak!”

Impairs: PDHC,aKGDH, bcaKADH

Question 20

What pathology of beri beri?

Answer 20

Nervous (strange eye movement)
Cardiac (heart failure)
if thiamine deficient

Question 21

Arsenic Poisoning: ARSENITE (trivalent)

Answer 21

Inhibits LIPOIC ACID: Decreased ATP Production:

Affects: PDHC, aKGDH, bcaKADH

Question 22

Arsenic Poisoning: ARESENATE (pentavalent)

Answer 22

Inhibits step 6 glycolysis

Decreased NADH and ATP production

Question 23

What is pathology of ARSENATE (pentavalent)

Answer 23

MEES’ Lines on nails

Nerve damage, Skin hyperkeratosis, cancer risk,

Question 24

4 sources of NADH?

Answer 24

1. aerobic glycolysis (malate shuttle)
2. PDHC
3. TCA
4. Beta Oxidation

Question 25

3 sources of FADH2?

Answer 25

1. Aerobic glycolysis (glycerol phosphate shuttle)
2. TCA (succinate dehydrogenase)
3. Beta Oxidation

Question 26

4 complexes of ETC?

Ndh(Sdh,g3p)CbcCaa3
(NFQCO) : N>F,F>Q,Q>C,C>O

Answer 26

1- NADdh- NADH to FMN
2- succinate-dh and glycerol-3p shuttle (FADH2 to CoQ)
3-cytochrome b/c1 (CoQ to Cytochrome C)
4-cytochrome a/a3 (cytochrome C to oxygen)

Question 27

3 Inhibitors/poisons of ETC

Answer 27

1. Cyanide (complex IV)
2. CO (complex IV)
3. Barbiturates (complex II)

Question 28

Antidote for Cyanide poisoning?

Answer 28

NITRITES- convert Hb (Fe2+) to metHb (Fe3+)

oxygen

Question 29

CO Poisoning

Answer 29

CO binds Hb displacing oxygen
OXYGEN TREATMENT

headache, nausea, tachycardia, tachypnea
red lips and cheeks,
respiratory depression, coma, death

Question 30

Uncouplers

Answer 30

ruin proton gradient but electron transfer is ok.
-Decreased ATP synthesis
-body compensates by trying to make more NADH and consumes more oxygen
_ENERGY RELEASED AS HEAT (b/c no atp synth)

Question 31

Natural uncoupler proteins (UCP: THERMOGENIN)

Answer 31

Found in brown fat of infants to keep them warm

Question 32

Why is brown fat brown?

Answer 32

High concentration of pigments in mitochondria from Cytochromes

Question 33

Hyperthyroidism and mitochondrial uncoupling

Answer 33

hyperthyroid can increase mitochondrial uncoupling

• TH may alter IMM
• TH may increase complex IV synthesis

Question 34

What is TCA and OP regulated by?

Answer 34

Oxygen and ADP mainly
decreased o2> decreased OP (increases NADH FADH2)
TCA inhibited via ICDH (respiratory control)

Question 35

Decreased oxygen has what affect on Oxphos

Answer 35

decreases OP but increases NADH FADH2
Inhibits TCA (known as respiratory control)

Question 36

When oxygen sufficient for Oxphos, then ADP regulates it.

high/low adp?

Answer 36

High ADP means low ATP

so - ADP activates TCA via ICDH to make more