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MCM Quiz 1 > TCA and OxPHOS > Flashcards

TCA and OxPHOS Flashcards

1
Q

What is the TCA cycle? where does it happen?

A

-Oxidizing carbon fuels for
harvesting high energy
electrons (e-)

-Source of precursors for
biosynthesis

-in mitochondria matrix!

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2
Q

Where doe Acetyl CoA come from?

A

Carbs, lipids, proteins

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3
Q

How does pyruvate enter TCA cycle and what happens to it?

A

using MPC,

PDC makes it acetyl CoA

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4
Q

What does PDC need to have to be used?

A

Needs TPP from 1 complex, needs to be dephosphorylated

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5
Q

What is the clinical significance of PDC?

A

-In a phosphatase deficiency PDC is always in
phosphorylated form

-Glucose becomes Lactate rather than
Acetyl CoA

-Results in constant lactic
acidosis

-Alanine intake should be
restricted

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6
Q

What is step 1 of TCA cycle?

A

Acetyl CoA + Oxaloacetate becomes citrate (citrate synthetase)

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7
Q

What is step 3 of TCA cycle? what is made

A

Isocitrate becomes a ketoglutarate (isocitrate dehydrogenase)

makes NADH and CO2

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8
Q

What is step 4 of TCA Cycle ? what is made

A

a ketoglutarate goes to succinyl CoA (a ketoglutarate deydrogenase)

makes NADH and CO2

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9
Q

what is the rate limiting step of TCA cycle

A

Isocitrate becomes a ketoglutarate (isocitrate dehydrogenase) step 2

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10
Q

Regulated steps?

A

1, 3 and 4

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11
Q

When is TCA cycle most active?

A

When ATP levels are low in the cell, high ATP is opposite

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12
Q

What aa fill up fumarate?

A

Phe Tyr Asp

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13
Q

What aa fill up oxaloacetate?

A

Asn Asp

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14
Q

What aa fill up a keto glutamate ?

A

Gln, Pro, His , Asg

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15
Q

What aa fill up succinyl coa?

A

Thr, Met, Ile, Val

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16
Q

What is citrate used to make?

A

fatty acids

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17
Q

what is malate used to make?

A

glucose

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18
Q

what is 2-Oxoglutaric aciduria?

A

A rare disorder with global
developmental delay and
severe neurological
problems in infants

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19
Q

what is Fumarase deficiency?

A

Issue with fumarase gene

Characterized by severe
neurological impairment.
Fatal outcome within the
first 2 yrs. of life

Increased urinary
excretion of fumarate,
succinate, aketoglutarate, and citrate

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20
Q

Oncometabolites of TCA cycle?

A
  • Citrate

- 2-hydroxyl glutarate

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21
Q

What does lower Eo mean?

A

has a lower affinity for
electrons; hence gives
them up easily to a redox
pair with a higher E0

inverse of G0

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22
Q

What is the purpose of Oxphos?

A

To transfer electrons from
NADH and FADH2 to O2

To establish a proton
gradient across the inner
mitochondrial membrane

To synthesize ATP

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23
Q

How does transfer of electrons work in oxphos?

A

The electron flows from the molecules with lower E0
to
that with highest E

ΔG0’ = -nƑ Δ E0

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24
Q

proton gradient established in oxphos? how?

A

Electron transfer through
the respiratory chain lead
to the pumping of H+ from
matrix to the innermitochondrial space

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25
Q

Two factors constitutes a

proton-motive force, what are they?

A

1) pH gradient (ΔpH)
2) Membrane
potential (ΔΨ)

26
Q

How is ATP synthesized in oxphos?

A

Catalyzed by a large
membrane-bound protein
• ATP synthase (Complex V)
uses pmf to make ATP

27
Q

Oligomycin disrupt what?

A

proton

transport through the complex v

28
Q

What does coenzyme Q do?

A

receives electrons from complex 1 and 2, passes them to complex 3

not a prosthetic group btw

29
Q

What does cytochrome c do?

A

takes electrons from complex 3, gives them to complex 4

30
Q

what happens when electron transport is prohibited?

A 
-A decrease in the
pumping protons
-A decrease in the
protein gradient
-Inhibition of ATP
synthesis
31
Q

what is oxphos sensitive to?

A
  • O2

- [ATP/ADP] ratio

32
Q

what does uncoupling do?

A

generates heat, not ATP made

-Protons (H+) reenter the mitochondrial
matrix from the intermembrane space
- TCA cycle and electron transfer to
O2 are accelerated

33
Q

What does Malate-aspartate shuttle do?

A

NADH cannot enter into mitochondria so it does it

Malate from cytosol enters mito, becomes oxaloacetate to release NADH, cycle starts again

Operates in the heart, liver, and
kidneys

34
Q

what does Glycerophosphate-shuttle do?

A

Generates FADH2
in the inner mitomembrane

Operates in skeletal muscle and
brain

35
Q

What is Luft’s Disease?

A

first mitochondrial disease ,
– Uncoupling of oxidative phosphorylation was found
– High levels of Cytochrome-c oxidase

36
Q

Causes of mitochondrial diseases

A

Primary cause :
– Defect in nuclear DNA (nDNA) encoding the mitochondrial proteins
– Defect in mitochondrial DNA (mDNA)

Secondary causes:
– Ischemia
– Reperfusion
– Cardiovascular diseases

37
Q

What do mitochondrial diseases look like?

A

– Nervous system: seizures,ataxia,dementia, deafness, blindness
– Eyes : ptosis, external ophtalmolplegia,retinis pigmentosa with visual loss
– Skeletal muscle : Muscle weakness, fatigue, myopathy, exercise
intolerance, loss of coordination and balance

– Low energy production
– Increased free radical production
– Lactic acidosis

38
Q

CoA what is it?

A

activator of acyl

groups

39
Q

Energy from glucose versus fatty acids

A

Fa have more energy. 36 in glucose vs 129 in pal acid

40
Q

Arsenite and lipoic acid ?

A

lipoic acid subunit (E2) of PDC is modified by arsenite , limits availability of lipoic acid

41
Q

Beriberi and Wernicke-Korsakoff ? why do they happen?

A

body does not
have sufficient thiamine

PDC doenst work well

42
Q

effects of citrate on rate-limiting enzymes?

A

High concentrations of citrate in a cell are indicative of an ATP-rich state, limits glucose catabolism

43
Q

Rat poison inhibits the TCA cycle , how?

A

Fluoroacetate is a rat poison that inhibits the TCA cycle

Fuoroacetate
reacts with CoA to form fluoroacetyl CoA, which (instead of acetyl CoA)
condenses with oxaloacetate to produce fluorocitrate

Inhibis aconitase, citrase accumulates

44
Q

Pyruvate carboxylase deficiency ?

A

A disruption in pyruvate carboxylase activity causes more pyruvate
to be converted to lactic acid than oxaloacetate, the fanner of which accu- mulates in the blood.

45
Q

what are ferredoxins?

A

electron carriers in p450 systems mito

46
Q

Ubiquinone radical , why is it relevant?

A

intermediate in the
transfer of electrons from CDmplex I to ubiquinone, as well as in the transfer from reduced ubiquinone to CDmplex Ill.

The ‘Q- can pass an electron
to 0 2 to generate the free radical superoxide ( ·O;Z) anion

47
Q

what is cytochrome c and what does it do?

A

Cytochrome-c., induces a cascade of biochemical
reactions that result in the activation of a subfamily of cysteine proteases called caspases

causes apoptosis, can be a marker for apoptosis

48
Q

LHON, what is it what does it do?

A

Complex 1 and 3 not working

Degenerated Optic nerve

49
Q

Leigh syndrome

A

Complex 1 and 4

weak motor skills

50
Q

What do ARAC and AZT do?

A

drugs that are uncouplers

51
Q

Chemisosmosis theory?

A

transfer of electrons down a chain releases energy

52
Q

what does rotenone do?

A

Rotenone is a potent inhibitor of NADH dehydrogenase (Complex I) of the mitochondrial electron
transport chain

53
Q

Respiratory chain components encoded by mtDNA ?

A

every complex but complex II

54
Q

Cyanide ? what does it do?

A

noncompetitive inhibitor of complex IV, rapid cell death

55
Q

aspirin overdose? what happens?

A

At high concentrations, salicylate uncouples oxidative phosphorylation by disrupting the
proton gradient across the inner mitochondrial membrane and causes
the dissipation of energy as heat

56
Q

Other electron transport systems?

A

P450, in ER, uses NADPH

57
Q

Nucleoside analogue treatments, what do they do?

A

The activated drugs inhibit mitochondrial DNA polymerase and deplete mitochondrial DNA.

As a result, the synthesis of locally produced components of the respiratory chain, particularly in CDmplex I, is inhibited, leading to a loss of ATP
production.

58
Q

what do Antiporters for phosphate/OH do?

A

phosphate imported in exchange for OH

59
Q

Antiporter for ADP / ATP exchange what does it do?

A

translocase moves one ATP out and one ATP into matrix

60
Q

Where do NADH and FADH2 come from?

A

NADH comes from TCA cycle, pyruvate oxidation and ketone body oxidation

FADH2 comes from multiple sources, such as succinate dehydrogenase

MCM Quiz 1 (9 decks)

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