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UT BCH 369 > Exam 3: Weeks 9-11 > Flashcards

Exam 3: Weeks 9-11 Flashcards

1
Q

citric acid cycle products

A

3 NADH, 1 FADH2, 1 GTP/ATP, 2 CO2

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2
Q

regulatory enzymes in citric acid cycle

A

isocitrate dehydrogenase (+ for ADP, - for NADH and ATP)

alpha-ketoglutarate dehydrogenase (- for NADH, ATP, succinyl CoA)

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3
Q

high succinyl coA will slow down…

A

ETC

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4
Q

dehydrogenase catalyzes…

A

an oxidation step

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5
Q

oxidation steps in citric acid cycle

A

4; 1 produces FADH2, 3 produce NADH

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6
Q

high ADP means energy is…

A

low

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7
Q

can i keep selling seashells for money officer?

A

pneumonic for citric acid cycle

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8
Q

acetyl-CoA starts the…

A

citric acid cycle

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9
Q

dehydrogenases in citric acid cycle

A

I AcKnowledge, SUCky Men

Isocitrate
Alpha-Keto
SUCcinate
Malate

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10
Q

ETC: 1 NADH creates…

A

2.5 ATP

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11
Q

ETC: 1 FADH2 creates…

A

1.5 ATP

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12
Q

proton gradient from ETC is in…

A

intermembrane space

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13
Q

NADH and FADH2 comes from…

A

mitochondrial matrix

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14
Q

complex I

A

NADH

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15
Q

complex II

A

FADH2

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16
Q

what happens to electrons as they pass through ETC?

A

they become lower and lower in free energy hence why they are passed on

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17
Q

final electron acceptor

A

removes low energy electron and binds them to free H+ to form water

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18
Q

synthesis of ATP in mitochondria is driven by…

A

a protein gradient

reoxidation of NADH and FADH2 indirectly creates a protein gradient

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19
Q

ATP synthase

A

“complex V”

carnival ride (subunit C) - loads H+ and rotates to power the rest

beta subunit - ATP produced

alpha subunit - stabilize the beta subunits

loose: ADP and inorganic phosphate (Pi) are mingling (ADP + Pi)

tight: ADP and Pi bind to produce ATP

open: ATP released

conformations change by rotating of the gamma stalk caused by rotating of C subunit

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20
Q

stator

A

holds ATP synthase in place

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21
Q

E cell

A

E red - (E ox)

PLUG IN AS GIVEN

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22
Q

what is oxidized? what is reduced? spontaneous reaction?

A

OIL RIG - use this to figure out what goes on which side of balanced equation

pick the half reaction with more negative potential (lower E value) will be oxidized

greater E value will be reduced

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23
Q

g deg: phosphorylase action

A

MAIN ENZYME: asdjfa;dkj

cleaves alpha 1,4 linkages and creates glu-1-phosphate

will cleave 7-8 glucose monomers (whatever is 4 monomers away from the branch)

glu-1-phos –> glu-6-phos by phos

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24
Q

phosphoglucomutase

A

g1p –> g6p

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25
branch of glycogen
alpha 1,6 linkage
26
g6p + water
glucose + inorganic phosphate
27
once glycogen cleaved by g1p...
4 glucose monomers still attached - NOT wanted! transferase! takes 3 from the end and puts on end of glycogen chain alpha 1,6 glucosidase cleaves using water to create FREE GLUCOSE with the one that remained after the transferase passed through
28
after degradation, phosphorylase...
keeps cleaving the glycogen chain until it reaches the core
29
glycogen synthesis
MAIN ENZYME: glycogen synthase first, need to activate! with UDP glucose (glucose + UTP = UDP) synthase transfers glucose from UDP glucose onto growing chain glycogenin is the CORE - autoglycosylation can also transfer glucose (essentially, can participate in chain elongation) adds 7-8 monomers to core long chain isn't convenient!! we must branch branching enzyme! takes added glucose monomers and creates alpha 1,6 linkage to the 4th carbon from the right end of the core next branching point much be at least 4 units away from the last branching points
30
a to b
covalent modification (something is getting phosphorylated)
31
T to R
allosteric modification (something about external factors will affect being pushed into these states)
32
most active
phosphorylase a (phosphorylated) in R state
33
least active
phosphorylase b in T state
34
T state
active site is covered
35
phosphorylase b
not phosphorylated
36
liver is source of...
glucose mobilized between meals; liver stores glucose phosphorylase a is dominant
37
muscle...
energy reserve for muscle control; muscle CANNOT supply glucose because it does not contain glucose-6-phosphatase phosphorylase b is dominant
38
high conc of glucose reverts...
R to T state since a high conc of glucose means that the liver doesn't need to call on glycogen stores
39
high AMP means we need energy
R state which pushes forward glycogen degradation
40
high ATP means...
energy is needed
41
what does protein kinase A do?
phosphorylates!!
42
reciprocal regulation of glu deg and syn
protein kinase A and protein phosphatase 1
43
protein kinase A
phosphorylates through turning on kinases glycogen phosphorylase (b-->a) glycogen synthase (a-->b) starts the breakdown of glycogen because we need energy in the form of free glucose phosphorylase <3 phosphorylation
44
protein phosphatase 1
dephosphorylates! glycogen phosphorylase (a-->b) glycogen synthase (b-->a) starts glycogen synthesis to make glycogen and remove stores of free glucose
45
hormones
act on kinases
46
insulin
means high glucose level start glucose synthesis glycogen synthase kinase!! will become inactivated when insulin is high to produce glycogen to keep synthase in the a state inactivated by covalent modification through phosphorylation
47
glucagon and epinephrine
send out same signal low glucose level (glucose is gone)
48
phosphorylatine
activates phosphorylase kinase BUT inactivates
49
glycogenesis enzymes
glycogen synthase branching enzyme
50
glycogenolysis
glycogen phosphorylase transferase alpha 1,6 glucosidase
51
PPP phases/products
phase 1: oxidative phase - make NADPH phase 2: non oxidative phase - makes 5C sugars (ribose-5-phosphate)
52
mode 1
when we need ribose 5 phosphate MORE than NADPH non-oxidative phase cell division since r5p is needed MUCH more
53
mode 2
need ribose 5 phosphate and NADPH equally oxidative phase then an isomerase to transform ribulose to ribose ex: when cell is rapidly dividing since r5p is needed for nucleotide materials and NADPH for biosynthetic needs - would more need r5p MORE but still "equal" - acceptable answer according to labrake
54
mode 3
need lots of NADPH >> r5p oxidative state - easy isomerase will create r5p but we do not need it! end up with glycolysis intermediates that can go into further oxidative steps go into gluconeogenesis (??) repeat until cell is happy needed when synthesizing fatty acids
55
mode 4
need NADP and ATP oxidative state glycolysis intermediates and go forth with glycolysis will create pyruvate for citric acid cycle and electron transport chain to make ATP needed during oxidative stress
56
NADPH
reduces reactive oxidative species
57
PPP effectors
NADP+ (+) fatty acid acyl CoA (-) NADPH (-)
58
first step of PPP
dehydration of glucose-6-phosphate
59
how much more ATP is generated from glucose-6-phosphate, compared to glucose, when it is metabolized by the glycolytic pathway?
1 glycolysis: 4 ATP products- 2 ATP react = 2 net ATP starting at g6p: 4 - 1 = 3 therefore 1 more is generated why? we skip the first reaction that takes an ATP (????)
60
glutathione protects against
reactive oxidative species
61
fatty acid synthesis
1. transport from mitochondria: acyl-conitine 2. activation
62
acc1 and 2
regulated covalently and allosterically
63
acc1
cytosol
64
acc2
mitochondria
65
inhibition of acc2 will...
push forward beta oxidation; therefore, negative effectors of acc2 will push it forward
66
fatty acid synthesis
acetyl coA in mitochondria is converted to citrate and transported to cytoplasm where it is reconverted
67
insulin dephos....
acc1 and acc2 become active
68
activation of FA
acyl-coA synthetase - ATP is required
69
steps of beta oxidation
oxidation hydration oxidation thiolase
70
products of beta oxidation
1 nadh, 1 fadh, 1 acyl coa
71
example where glucose in the body is low: prolonged starvation
ketone bodies can be used as alt source of energy! especially important for the brain! keto diet is meant for epilepsy
72
nutritional ketosis
not that bad but can't last forever because it makes the blood acidic
73
ketoacidosis
dangerous for individuals with type 1 diabetes
74
which ketone body contributes the most energy
3-hydroxybutyrate
75
complex that does not contribute to proton gradient
complex ii

UT BCH 369 (2 decks)

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