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MCM Quiz 1 > TCA and OxPHOS > Flashcards

TCA and OxPHOS Flashcards

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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
Two factors constitutes a | proton-motive force, what are they?
1) pH gradient (ΔpH) 2) Membrane potential (ΔΨ)
26
How is ATP synthesized in oxphos?
Catalyzed by a large membrane-bound protein • ATP synthase (Complex V) uses pmf to make ATP
27
Oligomycin disrupt what?
proton | transport through the complex v
28
What does coenzyme Q do?
receives electrons from complex 1 and 2, passes them to complex 3 not a prosthetic group btw
29
What does cytochrome c do?
takes electrons from complex 3, gives them to complex 4
30
what happens when electron transport is prohibited?
``` -A decrease in the pumping protons -A decrease in the protein gradient -Inhibition of ATP synthesis ```
31
what is oxphos sensitive to?
- O2 | - [ATP/ADP] ratio
32
what does uncoupling do?
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
What does Malate-aspartate shuttle do?
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
what does Glycerophosphate-shuttle do?
Generates FADH2 in the inner mitomembrane Operates in skeletal muscle and brain
35
What is Luft's Disease?
first mitochondrial disease , – Uncoupling of oxidative phosphorylation was found – High levels of Cytochrome-c oxidase
36
Causes of mitochondrial diseases
Primary cause : – Defect in nuclear DNA (nDNA) encoding the mitochondrial proteins – Defect in mitochondrial DNA (mDNA) Secondary causes: – Ischemia – Reperfusion – Cardiovascular diseases
37
What do mitochondrial diseases look like?
– 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
CoA what is it?
activator of acyl | groups
39
Energy from glucose versus fatty acids
Fa have more energy. 36 in glucose vs 129 in pal acid
40
Arsenite and lipoic acid ?
lipoic acid subunit (E2) of PDC is modified by arsenite , limits availability of lipoic acid
41
Beriberi and Wernicke-Korsakoff ? why do they happen?
body does not have sufficient thiamine PDC doenst work well
42
effects of citrate on rate-limiting enzymes?
High concentrations of citrate in a cell are indicative of an ATP-rich state, limits glucose catabolism
43
Rat poison inhibits the TCA cycle , how?
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
Pyruvate carboxylase deficiency ?
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
what are ferredoxins?
electron carriers in p450 systems mito
46
Ubiquinone radical , why is it relevant?
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
what is cytochrome c and what does it do?
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
LHON, what is it what does it do?
Complex 1 and 3 not working Degenerated Optic nerve
49
Leigh syndrome
Complex 1 and 4 weak motor skills
50
What do ARAC and AZT do?
drugs that are uncouplers
51
Chemisosmosis theory?
transfer of electrons down a chain releases energy
52
what does rotenone do?
Rotenone is a potent inhibitor of NADH dehydrogenase (Complex I) of the mitochondrial electron transport chain
53
Respiratory chain components encoded by mtDNA ?
every complex but complex II
54
Cyanide ? what does it do?
noncompetitive inhibitor of complex IV, rapid cell death
55
aspirin overdose? what happens?
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
Other electron transport systems?
P450, in ER, uses NADPH
57
Nucleoside analogue treatments, what do they do?
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
what do Antiporters for phosphate/OH do?
phosphate imported in exchange for OH
59
Antiporter for ADP / ATP exchange what does it do?
translocase moves one ATP out and one ATP into matrix
60
Where do NADH and FADH2 come from?
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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