Chapter 3 Study Questions (Part 5) Flashcards

1
Q

how does the lack of oxygen affect ETC? why?

A

can’t oxidize the last two transporters. shuts down.

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2
Q

how does the lack of oxygen affect chemiosmosis? why?

A

shuts down.

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3
Q

how does the lack of oxygen affect the TCA cycle?

A

shuts down. no pyruvate means FADH2 and NADH depleted, means no acetyl CoA, means can’t be oxidized.

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4
Q

how does lack of oxygen affect glycolysis and why?

A

nothing happens. it’s unaffected because glycolysis doesn’t use O2.

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5
Q

why does pyruvate build up in cells under anaerobic conditions?

A

not converted to acetyl, gets reduced to lactate instead.

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6
Q

what is the role of lactic acid fermentation?

A

regenerate NAD to keep glycolysis going. lactate is byproduct of it, that’s it.

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7
Q

when would we want to regenerate NAD+ ?

A

to run glycolysis under low oxygen conditions

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8
Q

describe the effect of regenerating NAD+ on O2 and CO2 levels

A

no O2 required, no CO2 produced

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9
Q

when tissue gets reoxygenated, what happens first?

A

ETC –> chemiosmosis –> oxidative phosphorylation

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10
Q

when tissue gets reoxygenated, what happens to NADH and FADH2?

A

they get oxidized

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11
Q

when tissue gets reoxygenated, what happens second?

A

TCA

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12
Q

when tissue gets reoxygenated, what happens to pyruvate levels and why?

A

you get back the pyruvate you lost earlier. it’s a reversible reaction taking place due to the law of mass action.

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13
Q

why is the amount of ATP produced from NADH made in glycolysis not always the same?

A
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14
Q

what happens after Fructose-1,6-Bisphosphate is made?

A

after F-1,6-BP is made, NADH passes its two electrons to make glycerol 3-phosphate. a transporter takes G3P across the outer mitochondrial membrane. pushing e- from NADH into cytosol, past the first mitochondrial membrane.

G3P passes the two electrons to make FAD to make FADH2, which remain embedded in the inner mitochondrial membrane

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15
Q

what does FADH2 do with its 2e-?

A

passes them to coenzyme Q in the inner mitochondrial membrane.

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16
Q

where is coenzyme Q located? why is that significant?

A

at stage 2. cause stage 2 does not pump H+. proton pumps that make the proton gradient are only located at ETC stages 1,3,4

17
Q

what happens to the e- that get unloaded at stage 2 of the ETC? why is that significant?

A

they only power the H+ pumps at stages 3 and 4. this produces a smaller proton gradient, and less protons to run through ATP synthase for ATP production

18
Q

which pathway of cellular respiration produces ATP the quickest?

A

glycolysis

19
Q

which pathway of cellular respiration produces the most ATP?

A

oxidative phosphorylation

20
Q

why is it said that triglycerides are guilt for energy storage?

A
21
Q

what are the different sources for gluconeogenesis?

A

1 is glycogen, glycerol.

minor: glycerol, lactate.

starvation conditions: protein.

22
Q

why can’t arbon from fatty acids be used to make glucose in gluconeogenesis?

A

carbons are lost as CO2

23
Q

why can’t acetyl CoA made from pyruvate be used to make glucose?

A

large NEGATIVE delta G aka not reversible!

24
Q

how can a protein be used to make glucose?

A

by recycling amino acid intermediates into the TCA cycle to make glucose

25
Q

what hormone is released in response to low blood glucose?

A

glucagon

26
Q

why do we need to maintain blood glucose levels?

A

body prefers glucose as energy source. especially brain. RBCs only do glycolysis

27
Q

what is B-oxidation?

A

B carbon is oxidized by exchanging the H for a doubled bond O

28
Q

why does excessive B-oxidation lead to keton body formation?

A

CoA removes one 2C acetyl group and leaves behind a new COOH end

29
Q

why does excessive B-oxidation lead to ketone body formation?

A

CoA removes one 2C acetyl group and leaves behind a new COOH end

30
Q

why is excessive ketone body formation potentially dangerous?

A

super acidic, can be lethal. overwhelms TCA and can’t go backwards.

31
Q

what energy soure can be used to make acetyl CoA to feed the TCA cycle?

A

at the beginning: glucose and fatty acids

in the middle: glucose, fatty acids, protein

32
Q

what is the warburg effect?

A

accelerated glycolytic pathway. the activity of major enzymes is accelerated.

33
Q

what are the three major enzymes involved in the glycolytic pathway?

A

PFK

pyruvate kinase

hexokinase

34
Q

what effect would a compound that inhibits PFK have on tumor growth and why?

A

limit PFK, limit speeding up back half

35
Q

what effect would a compound that inhibits pyruvate kinase have on tumor growth and why?

A

it’s like reverse mass action: slows down back half

36
Q

what does phosphofructokinase do?

A

rate determining step, mass action, commits glucose

37
Q

what does pyruvate kinase do?

A

intermediate of the front half speeds up the back half