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biochem > biochem lecture 4 pt 2 > Flashcards

biochem lecture 4 pt 2 Flashcards

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1
Q

what happens when there’s no O available

A

in order for cell to generate ATP in absence of oxygen there is a need for NAD+ (oxidized NAD)

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2
Q

what serves as an electron acceptor in redox rxn for G3P to 1,3-BPG

A

NAD+ (oxidized NAD)

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3
Q

what do we generate after NAD+ accepts electron

A

NADH

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4
Q

what is goal of fermentation

A

to regenerate NAD+

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5
Q

why is the goal of fermentation to generate NAD+

A

without that glycolysis won’t be able to continue

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6
Q

what happens to everything in the absence of oxygen

A

shut down TCA, ETC, ox phos

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7
Q

what happens to electrons in absence of O

A

no place for electrons to be donated to; no electron acceptor

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8
Q

basically what happens if no O2 available to keep redox balance

A

everything backs up and stops

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9
Q

what are fermentation reactions a way for

A

maintain redox balance so that you don’t have accumulation of NADH and everything stops

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10
Q

what happens if redox balance is disrupted

A

stuff accumulates and later stops

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11
Q

why does glycolysis continue when TCA cycle and ETC shut down

A

because in fermentation reactions you generate oxidized NAD+ which allows glycolysis to keep going

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12
Q

define fermentation

A

energy extraction (like ATP formation thru substrate level phosphorylation) w/o oxygen consumption

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13
Q

is there a net change in [ ] of NAD+ and NADH in fermentation

A

nope

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14
Q

basically what is fermentation

A

means by which ATP production (primarily thru substrate-level phos) occurs without consumption of oxygen

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15
Q

what happens cuz there’s no final electron acceptor in absence of oxygen

A

we are maintaining some redox balance by transferring electrons from NADH to something else

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16
Q

how do we maintain the redox balance in absence of oxygen

A

by transferring electrons from NADH to something else

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17
Q

what is that “something else” (that we transfer electrons from NADH to)

A

usually a product that’s generated at end of fermentation pathway –> ethanol or lactate

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18
Q

basically how does fermentation maintain redox balance

A

by transferring electrons from NADH to ethanol or lactate

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19
Q

describe lactic acid fermentation

A

conversion of glucose to lactate

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20
Q

how many steps in lactic acid ferementation

A

one step process

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21
Q

when does lactic acid fermentation occur

A

when we have oxygen depletion in muscle in mammals (extended muscle contraction)

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22
Q

what happens despite oxygen being depleted

A

doesn’t change the fact that muscle needs ATP E; just needs from a diff source

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23
Q

basically where is the ATP that muscle needs coming from (in short erm)

A

in lactic acid fermentation step

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24
Q

how many redox reactions in lactic acid fermentation

A

2 redox reactions

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25
is there a net change in oxidation state of carbons in glucose
nope; same H:C ratios for glucose and lactate
26
is there energy extracted in conversion of glucose to lactate
yup; 2 ATP per glucose
27
describe what happens to pyruvate at end of glycolysis in lactic acid fermentation
pyruvates at end of glycolysis are gonna be used in a redox reaction that oxidizes NADH to NAD+, and reduces pyruvate to lactate
28
what is the issue after glycolysis
NAD is reduced to NADH
29
what do we need to do to keep glycolysis going
find a way to oxidize NADH to NAD+
30
why do we say there is no net change in [ ] of NAD+ and NADH (oxidized vs. reduced NAD)
because the cell just cycles back between oxidized and reduced forms (basically we're carrying out cyclical redox reactions involving NAD)
31
what enzyme in lactic acid fermentation
lactate dehydrogenase
32
what does fermentation allow for
regeneration of NAD+ (oxidized) in order to extract energy (ATP) from glucose; no net change in [NAD+] and [NADH]; same ratios
33
what is the biggest takeaway in fermentation
need to regenerate NAD+
34
what happens without NAD+
we can't continue glycolysis
35
why is there no net change in NADH vs NAD+
b/c its just cycling b/w reduced and oxidized forms
36
what does oxidizing to NAD+ allow
keeps glycolysis going, enable cell to keep generating ATP in absence of oxygen
37
which generates more ATP, glycolysis (fermentation) or cell respiration
cell respiration by a lot, but still
38
describe fermentation as a solution
short-term solution
39
what happens in the long run
we will need oxygen at some point
40
describe ethanol fermentation
two steps, converts pyruvate --> acetaldehyde --> ethanol
41
what is first enzyme in ethanol fermentation
pyruvate decarboxylase
42
what does pyruvate decarboxylate do
pyruvate --> acetaldehyde; carries out a decarboxylation rxn where we release one of the Cs from pyruvate in the form of CO2
43
what does decarboxylation do
generates acetaldehyde intermediate
44
what is second enzyme
alcohol dehdyrogenase
45
what happens to acetaldehyde intermediate
goes thru redox reaction
46
describe alcohol dehydrogenase
same as lactate dehydrogenase
47
what does alcohol dehydrogenase do
regenerates oxidized NAD (so NAD+) ***CRITICAL STEP and reduces acetaldehyde to form ethanol
48
do lactic acid and ethanol fermentation have the same goals
yup; to reoxidize NAD so it can be fed back into glycolysis and keep it going
49
what does anaerobic fermentation lead to
production of 2 ATP/glucose
50
what does ox phos yield
up to 38 ATP/glucose
51
who gives more
ox phos (cell respiration)
52
what did Pasteur discover
yeast consumes a lot more glucose vs/ yeast grown in oxygen
53
pasteur effect
yeast cultures grown anaerobically are able to consume glucose via glycolysis a lot more glucose compared to aerobically
54
why do anaerobic yeast cultures consume more glucose
ramping up of glycolysis is a way of maintaining the same level of ATP in cell under anaerobic conditions vs aerobic
55
how do cells generate same numbers of ATP in absence of oxygen
by ramping up glycolysis; increasing production of glycolytic enzymes, increasing rate & level of glycolysis in cell
56
so who has more glycolytic activity
anaerobic conditions
57
what is pasteur effect
yeast consume more sugar when grown under anaerobic conditions
58
who has faster rate of ATP production
anaerobic glycolysis, up to 100x faster than ox phos (but uses way more glucose)
59
on an absolute scale who has more ATP
anaerobic glycolysis, but number of ATP per glucose is same (we also use more glucose)
60
who has more ATP per unit
both have same; 2 ATP per glucose
61
basically what is pasteur effect
we are increasing expression of enzymes that carry out steps of glycolysis
62
how is it the same ATP per unit
we feed more glucose into glycolysis
63
what 2 enzyme deficiencies affect enzymes that are in glycolytic pathway
hexokinase deficiency and pyruvate kinase deficiency
64
what step is hexokinase
first step
65
what step is pyruvate kinase
last step
66
what do both of these deficiencies do
affect our ability to transport, carry, deliver oxygen to tissues
67
what is responsible for oxygen transport & deliveries
red blood cells
68
why are red blood cells responsible
cuz they have a lot of hemoglobin
69
what is hemoglobin
oxygen binding protein
70
what is hemoglobin structure
tetrameric structure so its affected by allosteric mechanisms
71
where does the link between hemoglobin and glycolysis come from
an intermediate; 1,3-BPG
72
what does BPG have an effect on
hemoglobin's affinity for oxygen
73
where does BPG bind to hemoglobin
central portion of tetramer of hemoglobin (where the 4 subunits meet)
74
what's at the central portion
a lot of salt bridges, electrostatic interactions
75
what is result of BPG binding to hemoglobin
perturbs salt bridges, lowers hemoglobin's affinity for oxygen
76
describe BPG in normal conditions
BPG is an important player in facilitating dumping of oxygen into tissues that need it from hemoglobin
77
what do these two deficiencies do to BPG
altered levels of BPG
78
what does hexokinase do
reduced ATP and BPG production
79
describe hexokinase deficiency
can't convert glucose to G6P, since 1,3-BPG formation occurs after this step, if first step can't occur then 1,3-BPG is not formed
80
what does less BPG to do hemoglobin's affinity for oxygen
BPG binds to hemoglobin and lowers its affinity; less BPG increases hemoglobin affinity
81
what happens w/ increased hemoglobin affinity
hemoglobin needs to bind AND release oxygen; if too much affinity it can't release oxygen
82
basically what does less BPG do
greater affinity for oxygen, and thus harder to release
83
what kinda protein is hemoglobin
allosterically regulated protein
84
what kinda curves do we associate hemoglobin with
sigmoidal curves
85
what does oxygen binding to hemoglobin do
influences the affinity of binding of subsequent oxygens to other 3 subunits of tetramer
86
what curve associated w/ protein allostery
sigmoidal curve
87
sigmoidal curve is specifically associated with what
cooperativity allostery
88
what are cooperative effects
if we have a binding of ligand, it binds to 1 of 4 subunits. transmits conformational changes in tetramer that leads to elevation/increase in affinity of binding oxygen to other three subunits.
89
what is increase in affinity further increased with
each oxygen that binds
90
describe middle trace
normal; shallow slope
91
what happens to slope as you increase [ ] of oxygen
steepens a lot til it levels off
92
what happens in hexokinase deficient individuals
lowers BPG; increases affinity; leftward shift in curve
93
what does leftward shift mean
increased affinity (achieve same percent at lower value)
94
rightward shift
lowering of affinity (achieve same percent at higher value; takes more to achieve the same)
95
what is pyruvate kinase deficinecy
block occurs after step of BPG forms; buildup. concentrations of intermediates will increase, so more BPG
96
what happens to BPG levels in pyruvate kinase deficient ppl
higher levels of BPG
97
what does more BPG do
lowers hemoglobin's affinity for oxygen
98
what happens in both cases
problems in ATP production; reduction in O2 delivery, but for diff reasons
99
hexokinase
hemoglobin has too much affinity, hangs on to O very tightly, not much will be dumped off
100
pyruvaye
don't have enough O binding to begin with, so less is delivered
101
what do tumors have more of
enhanced glucose uptake & glycolysis rates
102
glucose uptake correlated w/
tumor aggressiveness and poor prognosis
103
what happens to cancer cells
grow more rapidly than blood cells that nourish them; starved for oxygen, need ATP
104
why do tumors have increased glycolytic capacity
uncontrolled cell division, need more ATP to carry out processes
105
what happens in tumors
hypoxia
106
what is hypoxia
low levels of oxygen
107
HIF 1
hypoxia inducible transcription factor
108
how are tumor cells clever
can adjust to hypoxic conditions
109
what does HIF 1 do
increase expression of glycolytic enzymes as well as various glucose transport proteins
110
GLUT
example of glucose transporter
111
what do tumor cells do under hypoxic conditions
increase rate of glucose uptake and rate of glycolysis
112
what does increasing glucose uptake and glycolysis allow tumors to do
enables these oxygen and nutrient starved tumor cells to keep growing and dividing
113
what else does HIF-1 do
increases expression of VEGF
114
VEGF
vascular endothelial growth factor
115
what does VEGF do
stimulates vascularization within the tumor
116
what does VEGF increase
angiogenesis
117
what does tumor need as it grows
needs a way to increase nutrient uptake and ATP
118
how does VEGF increase nutrient uptake
VEGF released by tumor cells stimulates vascularization or blood supply to growing tumor
119
what is VEGF triggered by
HIP-1
120
angiogenesis
formation of blood vessels
121
warburg effect
tumor cells increase rate of glucose consumption (have increased metabolic activity, increased levels of glycolysis)

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