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Medical Cell Biology and Genetics > L9- Kreb and ETC > Flashcards

L9- Kreb and ETC Flashcards

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1
Q

excess G-6-P can..

A

feed into the pentose phosphate pathway to produce NADPH for biosynthesis and 5C sugars
- stored as glycogen

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2
Q

both fructose and galactose can enter glycolysis via

A

some extra steps

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3
Q

which stage does kreb cycle begin

A

stage 3

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4
Q

at the end of glycolysis what are we left with

A

pyruvate (3C x 2)

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5
Q

what happens to pyruvate once it has been formed during glycolysis

A

is transported from cytoplasm across mitochondrial membrane into the matrix

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6
Q

which enzyme catalysis the combining of pyruvate + CoA +NAD+ to form Acetyl CoA

A

Pyruvate dehydrogenase (PDH)

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7
Q

pyruvate –> acetylCoA

A

3C to 2C

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8
Q

which cofactors does PDH require

A

FAD, thiamine pyrophosphate and lipoid acid- B-vitamins provide these factors

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9
Q

PDH catalysing pyruvate –> acetyl CoA is a ………. reaction

A

irreversible- releases CO2

–> key regulatory step

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10
Q

PDH is activated by

A
  • Pyruvate
  • NAD+
  • ADP
  • Insulin
  • CoASH (coenzyme A- free SH group)
  • Dephosphorylation
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11
Q

PDH is inhibited by

A
  • Acetyl-CoA
  • NADH
  • ATP
  • Citrate
  • Phosphorylation
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12
Q

the TCA cycle is also known as

A

the kreb cycle

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13
Q

kreb cycle is considered the

A

hub of metabolism

  • sugars
  • fatty acids
  • ketone bodies
  • amino acids
  • alcohol
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14
Q

where does the kreb cycle occur

A

in the mitochondrial matrix

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15
Q

acetyl converted to

A

2CO2–> by breaking C-C bonds in acetyl CoA

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16
Q

products of the kreb cycle

Glucose (6C) + 2 pyruvate (3C) + 2 acteyl CoA (2C) + TCA =

A

Products:

  • 6NADH
  • 2FAD2H
  • 2GTP (ATP equivalent)
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17
Q

kreb cycle is

A

oxidative and releases some energy (GTP)

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18
Q

kreb cycle is regulate by

A

high and and low energy compounds (ATP/ADP and NADPH/NAD+ ratio)

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19
Q

4 main step of kreb cycle

A
  1. broken all C-C bonds
  2. oxidised all the C-atoms to CO2
  3. broken all the C-H bonds
  4. Transferred all the H atoms (H+ and e-) to NADH + H and FADH2
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20
Q

NADH and FADH produced in the kreb cycle are used to power

A

ATP synthesis in the ETC

21
Q

what sort of reaction is the kreb cycle

A

substrate level phosphorylation

22
Q

what is stage 4 of catabolism

A

the electron transport chain

23
Q

what sort of reaction is the electron transport chain

A

oxidative phosphorylation

24
Q

where does ETC occur

A

inner membrane of the mitochondria- cristae

25
Q

during the ETC what happens to NADH and FADH2

A

re-oxidised–> to form more NAD+ and FAD+ which can be re-used

26
Q

what is required during ETC

A

oxygen

- - Electrons transferred from NADH and FADH2 to molecular oxygen

27
Q

two processes occur in ETC

A
  1. Electrons on NADH and FADH2 transferred through a series of carrier molecules to oxygens (Electron transport)
  2. Free energy released used to drive ATP synthesis (Oxidative phosphorylation)
28
Q

describe how the ETC works

A

Electrons from NADH are passed onto an electron carrier PTC1, this drives Hydrogen atom from the matrix into the inner membrane.
• Electrons are transferred through a series of carrier molecules (mostly within proteins) to oxygen with release of energy

29
Q

energy released during electrons transfer

A

1) 30% energy used to form proton gradient

2) the rest used to release heat

30
Q

[H+] gradient across inner mitochondrial membraner

A

proton motive force

31
Q

return of protons is

A

faired energetically by electrochemical potential

32
Q

how do protons return from the inner membrane space to the mitochondrial matric

A

via ATP synthase

33
Q

when H+ flows through ATP synthase down proton gradient

A

ATP synthesis

34
Q

which reducing powerful has more energy : NADH or FAD2H

A

NADH

  • NADH use 3 PTCs
  • FADH2 uses 2 PTCs
  • Greater PMF more ATP synthesised
35
Q

when ATP is high and ADP what occurs to ATP synthase

A

no substrate to synthesise ATP –> inward flow of H_ stops

–> conc of H+ in intramitochondrial space increases preventing further H+ primping- stop ETC

36
Q

example of ETC inhibitors

A

Cyanide and carbon monoxide

uncouplers

37
Q

ETC and Cyanide and carbon monoxide

A
  • Blocks electron transport e.g. prevents acceptance of electrons by oxygen
  • No oxidative phos- no ATP
38
Q

ETC and uncouplers

A
  • Increase permeability of the mitochondrial inner membrane to protons
  • Decreases proton gradient and therefore reducing proton motive force
  • No phosphorylation of ADP by ATP synthase
39
Q

Ox/Phos diseases

A

Genetic defects in proteins encoded by mtDNA (some subunits of the PTCs and ATP synthase)  decrease in ETC and ATP synthesis .

40
Q

brown adipose tissues contains a high conc of

A

thermogenin

41
Q

thermogenin

A

a UCP1 (uncoupling protein) –> naturally occurring uncoupling protein

42
Q

brown adipose tissue and its response to the cold

A

noradrenaline (norepinephrine) activates :

  1. Lipase which releases fatty acids from Triacylglycerol
  2. Fatty acid oxidation  NADH/FADH2  electron transport
  3. Fatty acids activate UCP1
  4. UCP1 transports H+ back into mitochondria
  5. So, Electron Transport uncoupled from ATP Synthesis.
  6. Energy of p.m.f. is then released as extra heat.
43
Q

family of UCPs

A

role in heat generation by uncoupling- may have other functions

44
Q

who has more brown adipose tissue

A

newborn infants and hibernating animals

45
Q

newborn infants

A

have lots of brown adipose around vital organs to maintain heat

46
Q

oxidative phosphorylation

A
  • requires membrane associated complexes e.,g. inner mito membrane
  • cannot occur in absence of oxygen
  • major process for ATP synthesis in cells requiring large amount of energy
47
Q

substrate level phosphorylation

A
  • requires soluble enzymes
  • can occur in absence of O2
  • minor process for ATP synthesis inc ells requiring large amounts of energy
48
Q

summary of ATP synthesis from glucose

A

glucose –> pyruvate –> 6CO2 and 6H20 + 32 ATP

Medical Cell Biology and Genetics (33 decks)

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