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biochem > biochem lecture 4 pt 2 > Flashcards

biochem lecture 4 pt 2 Flashcards

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
Q

is there a net change in oxidation state of carbons in glucose

A

nope; same H:C ratios for glucose and lactate

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26
Q

is there energy extracted in conversion of glucose to lactate

A

yup; 2 ATP per glucose

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27
Q

describe what happens to pyruvate at end of glycolysis in lactic acid fermentation

A

pyruvates at end of glycolysis are gonna be used in a redox reaction that oxidizes NADH to NAD+, and reduces pyruvate to lactate

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28
Q

what is the issue after glycolysis

A

NAD is reduced to NADH

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29
Q

what do we need to do to keep glycolysis going

A

find a way to oxidize NADH to NAD+

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30
Q

why do we say there is no net change in [ ] of NAD+ and NADH (oxidized vs. reduced NAD)

A

because the cell just cycles back between oxidized and reduced forms (basically we’re carrying out cyclical redox reactions involving NAD)

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31
Q

what enzyme in lactic acid fermentation

A

lactate dehydrogenase

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32
Q

what does fermentation allow for

A

regeneration of NAD+ (oxidized) in order to extract energy (ATP) from glucose; no net change in [NAD+] and [NADH]; same ratios

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33
Q

what is the biggest takeaway in fermentation

A

need to regenerate NAD+

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34
Q

what happens without NAD+

A

we can’t continue glycolysis

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35
Q

why is there no net change in NADH vs NAD+

A

b/c its just cycling b/w reduced and oxidized forms

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36
Q

what does oxidizing to NAD+ allow

A

keeps glycolysis going, enable cell to keep generating ATP in absence of oxygen

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37
Q

which generates more ATP, glycolysis (fermentation) or cell respiration

A

cell respiration by a lot, but still

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38
Q

describe fermentation as a solution

A

short-term solution

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39
Q

what happens in the long run

A

we will need oxygen at some point

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40
Q

describe ethanol fermentation

A

two steps, converts pyruvate –> acetaldehyde –> ethanol

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41
Q

what is first enzyme in ethanol fermentation

A

pyruvate decarboxylase

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42
Q

what does pyruvate decarboxylate do

A

pyruvate –> acetaldehyde; carries out a decarboxylation rxn where we release one of the Cs from pyruvate in the form of CO2

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43
Q

what does decarboxylation do

A

generates acetaldehyde intermediate

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44
Q

what is second enzyme

A

alcohol dehdyrogenase

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45
Q

what happens to acetaldehyde intermediate

A

goes thru redox reaction

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46
Q

describe alcohol dehydrogenase

A

same as lactate dehydrogenase

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47
Q

what does alcohol dehydrogenase do

A

regenerates oxidized NAD (so NAD+) ***CRITICAL STEP and reduces acetaldehyde to form ethanol

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48
Q

do lactic acid and ethanol fermentation have the same goals

A

yup; to reoxidize NAD so it can be fed back into glycolysis and keep it going

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49
Q

what does anaerobic fermentation lead to

A

production of 2 ATP/glucose

50
Q

what does ox phos yield

A

up to 38 ATP/glucose

51
Q

who gives more

A

ox phos (cell respiration)

52
Q

what did Pasteur discover

A

yeast consumes a lot more glucose vs/ yeast grown in oxygen

53
Q

pasteur effect

A

yeast cultures grown anaerobically are able to consume glucose via glycolysis a lot more glucose compared to aerobically

54
Q

why do anaerobic yeast cultures consume more glucose

A

ramping up of glycolysis is a way of maintaining the same level of ATP in cell under anaerobic conditions vs aerobic

55
Q

how do cells generate same numbers of ATP in absence of oxygen

A

by ramping up glycolysis; increasing production of glycolytic enzymes, increasing rate & level of glycolysis in cell

56
Q

so who has more glycolytic activity

A

anaerobic conditions

57
Q

what is pasteur effect

A

yeast consume more sugar when grown under anaerobic conditions

58
Q

who has faster rate of ATP production

A

anaerobic glycolysis, up to 100x faster than ox phos (but uses way more glucose)

59
Q

on an absolute scale who has more ATP

A

anaerobic glycolysis, but number of ATP per glucose is same (we also use more glucose)

60
Q

who has more ATP per unit

A

both have same; 2 ATP per glucose

61
Q

basically what is pasteur effect

A

we are increasing expression of enzymes that carry out steps of glycolysis

62
Q

how is it the same ATP per unit

A

we feed more glucose into glycolysis

63
Q

what 2 enzyme deficiencies affect enzymes that are in glycolytic pathway

A

hexokinase deficiency and pyruvate kinase deficiency

64
Q

what step is hexokinase

A

first step

65
Q

what step is pyruvate kinase

A

last step

66
Q

what do both of these deficiencies do

A

affect our ability to transport, carry, deliver oxygen to tissues

67
Q

what is responsible for oxygen transport & deliveries

A

red blood cells

68
Q

why are red blood cells responsible

A

cuz they have a lot of hemoglobin

69
Q

what is hemoglobin

A

oxygen binding protein

70
Q

what is hemoglobin structure

A

tetrameric structure so its affected by allosteric mechanisms

71
Q

where does the link between hemoglobin and glycolysis come from

A

an intermediate; 1,3-BPG

72
Q

what does BPG have an effect on

A

hemoglobin’s affinity for oxygen

73
Q

where does BPG bind to hemoglobin

A

central portion of tetramer of hemoglobin (where the 4 subunits meet)

74
Q

what’s at the central portion

A

a lot of salt bridges, electrostatic interactions

75
Q

what is result of BPG binding to hemoglobin

A

perturbs salt bridges, lowers hemoglobin’s affinity for oxygen

76
Q

describe BPG in normal conditions

A

BPG is an important player in facilitating dumping of oxygen into tissues that need it from hemoglobin

77
Q

what do these two deficiencies do to BPG

A

altered levels of BPG

78
Q

what does hexokinase do

A

reduced ATP and BPG production

79
Q

describe hexokinase deficiency

A

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
Q

what does less BPG to do hemoglobin’s affinity for oxygen

A

BPG binds to hemoglobin and lowers its affinity; less BPG increases hemoglobin affinity

81
Q

what happens w/ increased hemoglobin affinity

A

hemoglobin needs to bind AND release oxygen; if too much affinity it can’t release oxygen

82
Q

basically what does less BPG do

A

greater affinity for oxygen, and thus harder to release

83
Q

what kinda protein is hemoglobin

A

allosterically regulated protein

84
Q

what kinda curves do we associate hemoglobin with

A

sigmoidal curves

85
Q

what does oxygen binding to hemoglobin do

A

influences the affinity of binding of subsequent oxygens to other 3 subunits of tetramer

86
Q

what curve associated w/ protein allostery

A

sigmoidal curve

87
Q

sigmoidal curve is specifically associated with what

A

cooperativity allostery

88
Q

what are cooperative effects

A

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
Q

what is increase in affinity further increased with

A

each oxygen that binds

90
Q

describe middle trace

A

normal; shallow slope

91
Q

what happens to slope as you increase [ ] of oxygen

A

steepens a lot til it levels off

92
Q

what happens in hexokinase deficient individuals

A

lowers BPG; increases affinity; leftward shift in curve

93
Q

what does leftward shift mean

A

increased affinity (achieve same percent at lower value)

94
Q

rightward shift

A

lowering of affinity (achieve same percent at higher value; takes more to achieve the same)

95
Q

what is pyruvate kinase deficinecy

A

block occurs after step of BPG forms; buildup. concentrations of intermediates will increase, so more BPG

96
Q

what happens to BPG levels in pyruvate kinase deficient ppl

A

higher levels of BPG

97
Q

what does more BPG do

A

lowers hemoglobin’s affinity for oxygen

98
Q

what happens in both cases

A

problems in ATP production; reduction in O2 delivery, but for diff reasons

99
Q

hexokinase

A

hemoglobin has too much affinity, hangs on to O very tightly, not much will be dumped off

100
Q

pyruvaye

A

don’t have enough O binding to begin with, so less is delivered

101
Q

what do tumors have more of

A

enhanced glucose uptake & glycolysis rates

102
Q

glucose uptake correlated w/

A

tumor aggressiveness and poor prognosis

103
Q

what happens to cancer cells

A

grow more rapidly than blood cells that nourish them; starved for oxygen, need ATP

104
Q

why do tumors have increased glycolytic capacity

A

uncontrolled cell division, need more ATP to carry out processes

105
Q

what happens in tumors

A

hypoxia

106
Q

what is hypoxia

A

low levels of oxygen

107
Q

HIF 1

A

hypoxia inducible transcription factor

108
Q

how are tumor cells clever

A

can adjust to hypoxic conditions

109
Q

what does HIF 1 do

A

increase expression of glycolytic enzymes as well as various glucose transport proteins

110
Q

GLUT

A

example of glucose transporter

111
Q

what do tumor cells do under hypoxic conditions

A

increase rate of glucose uptake and rate of glycolysis

112
Q

what does increasing glucose uptake and glycolysis allow tumors to do

A

enables these oxygen and nutrient starved tumor cells to keep growing and dividing

113
Q

what else does HIF-1 do

A

increases expression of VEGF

114
Q

VEGF

A

vascular endothelial growth factor

115
Q

what does VEGF do

A

stimulates vascularization within the tumor

116
Q

what does VEGF increase

A

angiogenesis

117
Q

what does tumor need as it grows

A

needs a way to increase nutrient uptake and ATP

118
Q

how does VEGF increase nutrient uptake

A

VEGF released by tumor cells stimulates vascularization or blood supply to growing tumor

119
Q

what is VEGF triggered by

A

HIP-1

120
Q

angiogenesis

A

formation of blood vessels

121
Q

warburg effect

A

tumor cells increase rate of glucose consumption (have increased metabolic activity, increased levels of glycolysis)

biochem (15 decks)

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