Ox Phos Flashcards

(94 cards)

1
Q

ETC oxidizes

A

NADH & FADH2

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2
Q

ETC donates electrons to

A

O2

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3
Q

energy from O2 reduction is used by

A

ATP synthase to phosphorylate ADP to ATP

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4
Q

complex I

A

NADH acceptor

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5
Q

name of complex I

A

NADH dehydrogenase

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6
Q

draw out the four complexes and pathway

A

pg 4

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7
Q

CoQ transfers electrons to

A

cytochrome c

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8
Q

cytochrome c carries electrons to

A

complex IV

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9
Q

complex IV will reduce

A

O2 to water

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10
Q

in ox phos energy from NADH and FADH2 is used to make

A

ATP

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11
Q

draw out the four complexes and pathway

A

pg 4

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12
Q

what determines flow of electrons

A

reduction

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13
Q

electrons are transferred from low to

A

higher energy

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14
Q

for a negative delta G, need what E

A

positive

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15
Q

Delta E =?

A

E acceptor - E donor (pg 5)

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16
Q

the one that will acquire electrons is one with highest

A

reduction potential

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17
Q

Complex I has noncovalently bound

A

flavin mononucleotide

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18
Q

FMN stands for

A

flavin mononucleotide

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19
Q

FMN accepts

A

two electrons from NADH

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20
Q

in complex I Several iron-sulfur centers pass

A

one electron at a time toward the ubiquinone binding site.

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21
Q

draw out the Q cycle**

A

pg 10

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22
Q

which complex has cytochrome c

A

complex IV

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23
Q

what has more energy NADH or FADH

A

NADH - it has more substance/meat than FADH

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24
Q

what is ultimately driving the synthesis of ATP

A

the energy from the proton-motive force

there’s more H+ outside the inner membrane than inside

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25
translocation of how many protons fuels synthesis of one ATP
3
26
overal Delta G of oxidation of NADH to O2
-53 kcal/mol
27
overall delta G of oxidation of FADH2 to O2
-41 kcal/mol
28
each NADH yields how many ATP
2.5
29
what happens to the energy that isn't used by ox phos
heat - this is important to keep us warm
30
if we need energy, like when we exercise
Ox phos will increase
31
at rest, what happens to ATP hydrolysis, ADP, and proton influx
they all decrease
32
at rest, what happens to electorchemical gradient
increases
33
at rest, what happens to NADH and FADH2
they are not oxidized and inhibit enzymes that generate them
34
even with rapid muscle contraction, ATP levels
only drop 20%
35
when we exercise, what happens to calcium levels in cell
it allows contraction of muscle but also revs up making ATP
36
when we exercise we have connection b/w CNS, motor neurons and neuromuscular junction, in the process of the transition we use what as a way to depol the cell
calcium
37
creatine does what
phosphorylated to produce
38
phosphocreatine produces
creatine
39
what is moving b/w filament and mitochondria
creatine
40
what is the main way we produce ATP
ox phos
41
NADH has to be what in order for glycolysis to mvoe
oxidized
42
high levels of NADH vs. NAD+ what happens
make
43
which is faster anaerobic or aerobic
anaerobic
44
if NAD+ is not recovered what wil happen
glycolysis will cease
45
how NAD+ is recovered determines the fate of
pyruvate
46
inner mitochondrial membrane is impermeable to
NADH
47
what is the major shuttle in most tissues
glycerol 3 phosphate shuttl
48
what does glycerol 3 phosphate shuttle do
it shuttles things from cytosol to mitochondria, specifically electrons iself, not NADH
49
besides glycerol 3 phosphate shuttle, what is another shuttle?
malate-aspartate shuttle
50
look at and comprae the difference b/w the two shuttles
pg 21
51
when levels of citrate increase, what can happen
citrate can leave mitochondria and go to cytosol and go to phosphofructokinase-1
52
phosphofructokinase-1 is inhibited by
citrate
53
name a communication b/w TCA cycle and glycolysis
citrate will stop phosphofructokinase-1
54
if you inhibit the ETC it is a
toxic substance
55
why is cyanide poisioning toxic
CN- inhibits complex IV of the ETC
56
two places where carbon monoxide is toxic, one is blood and one is
blocks complex IV of ETC
57
what is the disease with earl onset progressive neurodegenerative disorder with characteristic neuropathology consisting of focal, bilateral lesions in one or more areas of the central nervous system, including brainstem, thalamus, basal ganglia, cerebellum, spinal cord.
leigh syndrome
58
how can leigh syndrome be caused by two different defects
pyruvate dehydrogenase & pyruvate carboxylase pyruvate carboxylase produces oxaloacetate. if body can't produce oxaloacetate, leads to problems in energy production. mutations in ox phos in any of the complexes can also cause leigh
59
mitochondrial mutations result in a rare form of
diabetes
60
what is Km of binding for ATP to bind to potassium channel
low affinity, so high km
61
inhibitors of the electron transport chain disrupt
oxidative phosphorylation
62
dinitrophenol
it diffuses the proton gradient. it take H from intramembrouns space and dissipates it, so what happens to ox phos? it goes away (or slows down or is less efficient)
63
how is dinitrophenol a diet pill
makes electron transport system slower, you will lose weight, why? if you disconnect the ETC from ox phos, you can't make fat. so you will lose a LOT of weight.
64
cyanide binds to
Iron in heme of cytochrome c oxidase
65
what does pt take if they have cyanid poiionisng
vitamin B 12
66
how does vitamin b12 help with cyanide poision?
vitamin b 12 has very high affinity for cyanide, so you get rid of cyanide
67
acute exposure to high HCN
gives brief CNS stimulation followed by convulsion, coma & death.
68
acute exposure to low HCN
light-headedness, breathlessness, dizziness, numbness, headaches.
69
if you expend ATP fast (like shivering), what happens to electron transport system?
it has to work fast
70
how does shivering produce heat
ETC is not efficient, 70% goes to heat. so it's used as a tool to heat the body
71
non-shivering thermogenesis
person taking dnp will make the ETC work more and produce heat
72
succinate activates
complex II
73
ATP synthesis requires
electron transport
74
what happens to oxygen in complex IV
it is reduced
75
how many electrons does it take to reduce oxygen in complex IV
4
76
in complex IV what happens with hydrogen
four protons are pumped from matrix to intermembrane space
77
when are protons pumped across the membrane during ox phos
as electrons move through complexes I, III, & IV
78
how many total protons are passed for each NADH molecule reduced
10
79
the electrochemical gradient couples the rate of ETC to the rate of
ATP synthesis
80
inhibition of oxphos leads to accumulation of
NADH
81
any inhibition of the ETC inhibits
ATP synthesis, b/c they are tightly coupled
82
name some inhibitors of ETC
``` amytal rotenone Antimycin A CN- CO H2S NaN3 ```
83
explain how mitochondrial mutations result in rare form of diabetes
if you have defects in ox phos, you can't make ATP (or don't make enough) and then you can't depol the membrane, and then Ca2+ won't cause insulin to be released. pg 25
84
what is the function of ATP synthase
makes ATP, uses ADP + H+ to make ATP
85
if protons are leaked back into matrix w/out going through ATP synthase, what happens
dissipates the electrochemical gradient without ATP production
86
uncoupling of ox/phos and ATP results in what
increased oxygen consumption and heat
87
does electron transport require ATP synthesis
no
88
what is an example of a chemical uncoupler
DNP
89
how does DNP work
it is a chemical uncoupler it allows electrons to pass through gradient without producing ATP. your body burns more fat to keep energizing body
90
what does DNP stand for
dinitrophenol
91
compare contrast WAT vs. BAT
white: one lipid droplet, mitochondria & nucleus squeezed to layer near membrane brown: small and many lipid droplets. function: create heat. more mitochondria. more cytochrome for brown color.
92
how does BAT produce heat
it acts as uncoupling protein → thermogenesis
93
as energy is released in tissues by ATP hydrolysis, what increases
ADP
94
when you have accumulate NADH, describe chain of events that occurs
block OxPhos, backs up and blocks PFK-1 and inhibits glycolysis.