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Chem 153a > metabolic regulation > Flashcards

metabolic regulation Flashcards

1
Q

How is the ETC/ATP synthase regulated? including consequences of inhibition

A

negative: ATP
pos: ADP + Pi
consequences of inhibition: accumulation of NADH

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2
Q

how is alpha-ketoglutarate DH regulated? including consequences of inhibition

A

neg: NADH
pos: none
consequences of inhibition: lower oxaloacetate

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3
Q

how is isocitrate DH regulated? including consequences of inhibition

A

neg: NADH, ATP
pos: ADP
consequences of inhibition: accumulation of citrate

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4
Q

how is citrate synthase regulated? including consequences of inhibition

A

neg: NADH and citrate
pos: acetyl coa and oxaloacetate
consequences of inhibition: accumulation of acetyl coa

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5
Q

how is pyruvate dh regulated?

A

neg: NADH, acetyl coa
pos: ADP, pyruvate

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6
Q

how is pyruvate kinase regulated?

A

neg: ATP, NADH, acetyl coa
pos: F-1,6-BP

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7
Q

how is PFK regulated? including consequences of inhibition

A

neg: ATP, citrate
pos: AMP
consequences of inhibition: lower F-1,6-BP and accumulation of G-6-P

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8
Q

how is hexokinase regulated?

A

neg: G-6-P

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9
Q

which steps in glycolysis are regulated?

A

hexokinase, PFK, PK

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10
Q

which steps in TCA cycle are regulated?

A

citrate synthase, isocitrate DH, alpha-KGDH

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11
Q

Which enzymes does ATP inhibit?

A

PFK, OK, Citrate synthase, IDH, a-KGDH

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12
Q

Which enzymes for NADH inhibit?

A

PK, PDH, citrate synthase, IDH, a-KGDH

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13
Q

Which enzymes do ADP/AMP activate?

A

PFK, PDH, IDH, citrate synthase, a-KGDH

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14
Q

which enzyme does ADP inhibit?

A

PDH-K

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15
Q

How is the ETC regulated?

A

(+) ADP + Pi

(-) ATP

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16
Q

What does G-6-P inhibit?

A

hexokinase

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17
Q

What does citrate inhibit?

A

PFK and citrate synthase

18
Q

what does acetyl-coa inhibit?

A

PK, PDH

19
Q

what does succinyl coa inhibit?

A

a-KGDH and citrate synthase

20
Q

which part of the TCA cycle is regulated mainly by substrate availability?

A

citrate synthase from acetyl-coa and oxaloacetate

21
Q

How is PDH regulated?

A

inhibited by PDH kinase (which is activated by NADH and acetyl coa)
activated by PDH phosphatase (which is activated by insulin)

22
Q

What are the two ways that electrons from NADH in the cytosol can enter the electron transport chain?

A

Malate aspartate shuttle and glycerophosphate shuttle

23
Q

What are the benefits of the malate aspartate shuttle?

A

more efficient, because NADH is converted back to NADH, so no ATP is lost

24
Q

What are the benefits of the glycerophosphate shuttle?

A

Faster because e- are passed directly to an FAD in the inner membrane and the ETC but less efficient because NADH –> FAD means you get less ATP from it

25
Q

How does Pi from the cytosol enter the mitochondria?

A

through an H+/Pi symporter

26
Q

How does the H+/Pi symporter affect ATP synthase?

A

the H+ go with the pH gradient, thus reducing the H+ gradient used to drive ATP synthase, thereby reducing the energy available for ATP synthesis

27
Q

How does the Q cycle contribute to the generation of a proton gradient?

A

Oxidation of CoQH2 on IMS side releases protons to IMS. CoQ is always reduced on matrix side, so it releases protons from matrix to the IMS.

28
Q

Why does Q cycle contribute more to proton gradient than direct oxidation?

A

Undergoes multiple oxidations and one then gets rereduced so it leads to two more protons pumped

29
Q

How does a proton wire work

A

conformational changes due to e- transfer cause a series of nonconsecutive protonations and deprotonations of amino acid side chains which result in the net transfer of a proton from the matrix to the IMS

30
Q

What makes FMN and CoQ special electron carriers/acceptors

A

can accept or transfer 1 or 2 e- at a time

use a transient free radical intermediate (semiquinone)

31
Q

How many e- can NAD+ carry

A

obligated to carry 2e-

32
Q

how many e- can cytochromes carry/transfer

A

usually 1

33
Q

describe structure, location, and mechanism of electron transfer for CoQ

A

organic, lipid soluble molecule
located in the mitochondrial inner membrane
transfers 2 e- from C1 or 2 to C3 and carries 2H+ from matrix to IMS

34
Q

describe structure, location, and mechanism of electron transfer for cytochrome C

A

water soluble protein with a heme prosthetic group
found in IMS
carries 1 e- from C3 to C4

35
Q

What allows cytochromes to have different reduction potentials

A

the different microenvironments of the heme groups and the varying microenvironments of the proteins themselves

36
Q

what is an advantage of the Q cycle in C3

A

allows for 4H+ to be pumped into IMS instead of 2 from direct oxidation

37
Q

how are protons pumped in each complex of ETC

A

1: proton wire
2: not
3: Q cycle
4: proton wire

38
Q

What is the chemiosmotic hypothesis?

A

during the ETC, protons are transferred from the mito matrix to the IMS, generating a proton gradient. The dissipation of this drives ATP synthesis

39
Q

experimental observations which support chemiosmotic theory

A

a. Can measure the pH gradient across the mitochondrial inner membrane (membrane is impermeable to ions)
b. Artificial pH gradient results in ATP synthesis
c. Electron transport acidifies the cytosol
d. ATP synthesis requires intact mitochondria
e. Agents which destroy the pH gradient (uncouplers) prevent ATP synthesis

40
Q

where is Fo subunit located and what does it do

A

transmembrane unit which converts flow of protons into mechanical movement

41
Q

How is mechanical movement from Fo converted to ATP

A

communicated down the stalk portion to F1 unit which triggers conformational changes to drive ATP synthesis

42
Q

Where is F1 subunit located and what does it do

A

soluble unit in mitochondrial matrix and faciliatates conformational changes to drive ATP synthesis

Chem 153a (8 decks)

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