ETC and Oxidative Phosphorylation Flashcards

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1
Q

where is NAH and FADH2 produced?

A

in the mitochondrial matrix by catabolic processes (glycolysis, PDH, TCA cycle)

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2
Q

What is electron transport ?

A

moving electrons of the NADH or FADH2 (high energy compounds) along the inner mitochondrial components that are fixed in the membrane

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3
Q

what is oxidative phophorylation?

A

converting energy into energy that can be synthesized into ATP from ADP

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4
Q

what complexes contain iron-sulfur proteins? why is it important?

A

complex I, II and III

dynamic role in electron transfer process

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5
Q

what does hypoxia do to the ETC?

A

decreases the rate of ETC and ATP production
a drop in cellular ATP increases anerobic glycolysis and lactic acid production– anerobic glycolysis cannot meet most tissue demands

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6
Q

what can results from hypoxia?

A

myocardial infarction - tissue damage, leakage of enzymes (CK 1,2,LDH) and triponin I and T

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7
Q

Which molecule has the highest energy and lowest?

A

ATP, ADP, AMP

ATP - highest = more negative delta G
AMP - lowest

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8
Q

where does ETC and OP happen?

A

inner mitochondria membrane

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9
Q

what is the purpose of ETC?

A

make ATP from ADP using NADH and FADH2

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10
Q

what is the final proton acceptor and product?

A

oxygen

water

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11
Q

at what complexes are protons pumped into intrermembrane space

A

complex 1,3, 4

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12
Q

when will ETC be active?

A

high NADH/NAD+ ratio

Low ATP/ADP ratio (or high ADP)

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13
Q

Where is malate transproted?

A

into the mitochondria

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14
Q

where is aspartate transported?

A

out of the mitochondria

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15
Q

what phospholipid is essential for functioning of the ETC?

A

cardiolipin

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16
Q

what part in the ETC can an electron be lost and a superoxide may be formed?

A

at CoQ - entry point of electrons from glycerolphophate shuttle

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17
Q

when is the only time the heme groups intereact with molecular oxygen?

A

complex IV - the other complexes they just transport electrons

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18
Q

Name eight drugs or compounds that inhibit the ETC.

A

The ETC is inhibited by Amytal, Rotenone , Pericidin A, Antimycin A, Sodium azide, cyanide, carbon monoxide and hydrogen sulfide.

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19
Q
  1. Name 2 inhibitors of ADP-ATP translocase
A

The ADP-ATP translocase is inhibited by the toxins from plants like atractyloside and bongkrekic acid.

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20
Q
  1. How can ATP formation be described using the Mitchell’ Chemiosmotic theory?
A

The generation of a proton gradient by complex I, III and IV allows the usage of the energy of the generated proton gradient when the protons flow back into mitochondria through ATP synthase.

The energy generated by the proton gradient is enough to perform the ATP generation by ATP synthase, however, the ATP formation has to be connected to the ETC transport chain.

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21
Q

list the 7 diseases involving mutation in mitochondrial DNA

A
Leber Hereditary Optic Neuropathy 
Myoclonic epilepsy
Ragged-Red Fiber Disease 
MELAS
Aminoglycoside Induced Deafness
Rhabdomyolysis
Leigh disease (neurological disorder due to mutation of PDH, ETC or ATP synthase, nuclear and mtDNA can be affected)
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22
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex I and II?

A

FMN and FAD

22
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex III ?

A

heme group Fe3+

23
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex IV?

A

Cu2+ and heme group Fe3+

23
Q

what direction is DHAP going?

A

out of the mitochondria

24
Q

what drieciton is G-3-P going>

A

into the mitochondria

24
Q

how many ATP does NADH

A

3 ATP in Malate aspartate shuttle

2 ATP in glycerol phosphate shuttle

25
Q

how many ATP does FADH2 equal?

A

2 ATP

25
Q

when will ETC be active?

A

high ADP and high NADH

26
Q

what does hypoxia do to the ETC?

A

decreases the rate of ETC and decrease ATP formation = anaerobic glycolysis can’t handle it -= MI

26
Q

what drieciton is G-3-P going>

A

into the mitochondria

27
Q

how many ATP does NADH

A

3 ATP in Malate aspartate shuttle

2 ATP in glycerol phosphate shuttle

27
Q

how many ATP does NADH

A

3 ATP in Malate aspartate shuttle

2 ATP in glycerol phosphate shuttle

28
Q

how many ATP does FADH2 equal?

A

2 ATP

28
Q

how many ATP does FADH2 equal?

A

2 ATP

29
Q

when will ETC be active?

A

high ADP and high NADH

29
Q

when will ETC be active?

A

high ADP and high NADH

30
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex I and II?

A

FMN and FAD

31
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex III ?

A

heme group Fe3+

32
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex IV?

A

Cu2+ and heme group Fe3+

33
Q

what direction is DHAP going?

A

out of the mitochondria

34
Q

what drieciton is G-3-P going>

A

into the mitochondria

35
Q

how many ATP does NADH

A

3 ATP in Malate aspartate shuttle

2 ATP in glycerol phosphate shuttle

36
Q

how many ATP does FADH2 equal?

A

2 ATP

37
Q

when will ETC be active?

A

high ADP and high NADH

38
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex I and II?

A

FMN and FAD

39
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex III ?

A

heme group Fe3+

40
Q

what are the prosthetic groups (reversibly accept and donate electrons) in complex IV?

A

Cu2+ and heme group Fe3+

41
Q

what direction is DHAP going?

A

out of the mitochondria

42
Q

what drieciton is G-3-P going>

A

into the mitochondria

43
Q

how many ATP does NADH

A

3 ATP in Malate aspartate shuttle

2 ATP in glycerol phosphate shuttle

44
Q

how many ATP does FADH2 equal?

A

2 ATP

45
Q

when will ETC be active?

A

high ADP and high NADH

46
Q

what does hypoxia do to the ETC?

A

decreases the rate of ETC and decrease ATP formation = anaerobic glycolysis can’t handle it -= MI