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258: Physiology > lecture 6+7:summary oxidative, Regulation of the ETC and start of blood glucose > Flashcards

lecture 6+7:summary oxidative, Regulation of the ETC and start of blood glucose Flashcards

1
Q

what is the process of ETC and energy made called

A

oxidative phosphorylation

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2
Q

what are the 4 points of summary of oxidative phospogrylation

A

1) electron transport (in pairs) down the ETC from MADH or FADH2
2) Complex 1, 3 and 4 pump protons out of mito matrix to the intermembrane space (against a gradient, get energy from the electrons)
3) the pumping of the protons (h) cause a high concentration of protons and an electical potential=electrochemical gradient
4) the H+ flow back into matrix through atp synthase drives atp synthesis

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3
Q

when hydrogen protons are pumped into the intermembrane space , is it down or against their chemical gradient

A

against their concentration gradient which is why they need e nergy from electrons

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4
Q

explain the general carbon flow for glycolysis

A

glucose (6C) > 2 pyruvates (3C)

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5
Q

How many NADH do you form from glycolysis

A

2 NADH

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6
Q

What is the ATP produced for glycolis (without oxydative phos)

A

2 atp

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7
Q

What is the ATP produced for glycolis (with oxydative phos)

A

2 NADH molecules made from glycolysis go into oxidative phos. and make 6 atp total

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8
Q

what is the total theoretical yield for glycosis (with ETC)

A

8 atp

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9
Q

what is the general carbon flow for the pyruvate oxidation

A

2 pyruvates (3 carbon) > 2 acetyl coa (2 carbon)

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10
Q

how many NADH are produced from pyruvate oxidation

A

2 nadh (1 per pyruvate)

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11
Q

what is the atp yield for just pyruvate oxidation (wihtout ETC)

A

none

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12
Q

what is the yield of atp from pyruvate oxidation going to ETC

A

2 NADH go into ETC

6 atp are made

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13
Q

what is the total theoretical yield for pyruvate oxidation

A

6 atp

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14
Q

wht is the general carbon flow for kreb cyclem

A

2 acetyl coa (2 C) > 4 CO2

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15
Q

how many nadh and fadh2 are producted in the kreb cycle (for 2 acetyls)

A

6 nadh

2 fadh2

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16
Q

what is the atp yield solele from kreb cycle (without ETC)

A

2 atp

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17
Q

what is the atp yield for kreb cycle going into ETC only

A

6 nadh will give you 18 atp

2 fadh2 will give you 4 atp

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18
Q

what is the total theoretical yield for kreb cycle (with etc and alone)

A

24 atp

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19
Q

what is the general carbon flow for areboic glycolysis (everyhing together)

A

glucose (6 C) > 6 CO2

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20
Q

what is the total FADH2 and NADH made from all 3 processess (glycolysis, pruvate oxi and kreb)

A

10 nadh

2 fadh2

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21
Q

what is the net atp yield from substate phosphoraltion of all 3 processess only

A

4 atp

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22
Q

net atp yield through the oxidative phosphtation of the 3 processes

A

34 atp

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23
Q

what is the net yield maximum of all three processes

A

38 atp

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24
Q

where does the oxygen come from for the ETC

A

comes from circulation

o2 hemoglobin blood

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25
Q

where is CO2 in the 3 different processess

A

2 co2 for 2 pryvates to acetly

4 co2 for kreb cycle

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26
Q

what are some different functions for ATP

A

muscles (contraction)
nerve (actvie ion transport)
protein building (syntehsis of new molecules or cell grouwth and division)

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27
Q

what are some ways we can be lacking oxygen for the electron transport

A

during exercise
during high altitude
blood circulation problems

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28
Q

what is the net atp for anerobic glycolis

A

2 atp

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29
Q

what are the 2 factors taht positively influence the ETC

A 
aerobic exercise (training at better oxygen utilization) 
High intensity interval training (adaptations of mitochondira)
30
Q

what are the 4 inhibirors (negatively affect) the ETC

A
  • Cyanide
  • Olygomyosin
  • Carbon monoxide
  • Rotenone
31
Q

what is olygomysion

A

antibiotic

32
Q

what does CN stand for

A

cyanide

33
Q

what does CO stand for

A

carbon monoxide

34
Q

what is rotenone

A

pesticide

35
Q

which is the least lethal inhibitor of the ETC

A

carbon monoxide

36
Q

where does rotenone affect and what does it do

A

inhibits electron transport at complex 1
=block all downstream electron activity (electrons cannot transfer) hydrogens will not be able to go through and atp synthesis will cease

37
Q

where do cyanide and carbon monoxide affect the ETC and how

A

they inhibit eclectron transport chain at complex 4
it does not allow electrons to go to oxygen
since no hydgens can bind with oxygen, oxygen will build up in the cell and will become a radical form which can cause metabolic demage to the metichondria

38
Q

where does olygomision inhibit the ETC and how

A

blocks the ATP synthase molecule (inhibits hydrogens from coming back through the membrane so no ATP would be formed

39
Q

what do uncoupler poisins do and give an example

A

they carry alot of the protons into the matrix (=taking away from intermebrane space )
Heat is going to be formed and REDUCED ATP

40
Q

explain oligomyosin and relationship with cancer

A

oligomyosin is an antibiotic that can be given to cancer patients to kill the mitochondira of cancer cells
(but is also killing off alot of healthy cells)

Research is being used to only use the root of it that will kill mostly bad cells but can effect healthy cells like hair)

41
Q

explain the consequence of CN toxicity

A

CN binds to cytochrome oxidaze (complex 4) which blocks the pairs of electrons causing an increase in pairs of electrons
This electron pairing blockage will impeded hydrogens from going up (killing elecrochemical force)
Since there is buildup of H, FADH2 and NADH concentration will rise sinxe they cannot be oxidized
IF there is an increase of FADH2 and NADH, kreb cycle will be inhibited
If kreb cycle is inhibited, acetyl coa will buildup since it cannot go through the process
if acetyl coa builds up ,pyruvate is not going to goto acetyl coa and instead will move towards lactate

=BUILD UP OF LACTATE
=LACTIC ACIDOSIS

Also, no electrons will be binding with oxygon cause and increase in free radicals which is damaging to the cell

42
Q

how will increasing the amount of hydrogen in the cell affect ph

A

ph will decrease and will decrease cell metabolism causing cell death

43
Q

explain lactic acidosis

A

high levels of lactic acid (brought on by CN binding onto the complex 4) which can poisin your cell and decrease oxidative phosoho.

44
Q

what is DNP (name )

A

2.4 dinitrophenol

45
Q

true or false: DNP can easiliy diffuse though the inner mito membrane

A

true

46
Q

what is DNP (in terms of poinsin)

A

uNCOUPLER

47
Q

is DNP lipophillic or hydrophobic

A

lipophillic (easily diffuse through membrane)

48
Q

What is important about DNP in terms of ints structure

A

has a spot to bind hydrogen

49
Q

What is the poisin that used to be used for weight loss

A

DNP

50
Q

Explain the consequence of DNP (in terms of body weight)

A

DNP binds the hydrogen on itself and diffuses through the membrane (a lot of hydrogen diffuses through)
=loss of electrochemical gradient
=ATP production will drop significantly

DECREASE IN ENERGY CHARGE. AMP concentration in the cell will increase which will speed up glycolysis and lipolysis (breaking down the carbs and fats for energy in absence of ETC)
=loss of body weight

Because of the increased breakdown of carbs and fats, FADH2 and NADH will increase which means Electons are still going through even without the ATP production and because of this, heat is being produced in the mitochondra cause the cell temperature to increase
=HYPERTHERMIA

51
Q

what are the 2 affects on the mitchondira when you do aerobic training

A

1) increase the mitochondrial size

2) increase in mitcondrial number

52
Q

how does an increase in mitochondiral size positively affect ETC

A

by increase mitochondira size, you are increasing the size of the inner mictohondiral membrane
=Electron transport chain will get larger
=consume more oxygen, produce far more atp

53
Q

how does an increase in mitochondira number positively effect the ETC

A

More mitocondrials, you need greater oxygen consumption

with greater oxidative consumption, you will get an increase in number of atp

54
Q

what is the clinical application of aerobic training vs mitchondira

A

you will need ore oxygen and produce more atp

=INCREASE IN VO2 MAX

55
Q

does skeletal muscle have the necessary enzymes to allow glucose to go back into the circulatoon

A

no

56
Q

what is the enzyme responbible for allowing glucose 6 phospohate to go to glucose in the liver

A

glucose 6 phosphotase

57
Q

what is the purpose of gluconeogenesis

A

maintain circulating blood glucose levels by manufactoring glucose from the liver
(ie. when you feel hypoglycemic the liver will sense this and produce more glucose in the circulation)

58
Q

what is the chief organ important for maintenace of blood glucose level

A

LIVER

59
Q

what is normal blood glucose values

A

4-8 MM

60
Q

what are the 3 precursors to gluconeogenesis

A

lactate
glycerol
alanine

61
Q

where does lactate come from to get into circulation

A

skelteate muscle

62
Q

where does alanine come from to get into circulation

A

proteins

63
Q

where does glycerol come from to get taken up in circualtion

A

adipocytes

64
Q

How is alanine important for gluconeogenisis (structure)

A

Alanine has 3 carbons and a nitrogen group
just need to get rid of nitrogen group and it can become pyruvate which can become glucose 6 phospjate and then help in gluconegoenies

65
Q

true or false, pyruvate can easily turn into glucose 6 phosphate

A

true

66
Q

what is the process of pyruvate (from diff sources) going to glucose 6 phosphate and then out as glucose called

A

gluconeogenesis

67
Q

how is glycerol important for gluconeogeneis (structure)

A

Glycerol can also be taken up into the liver from a different metabolic pathway and become glucose

68
Q

how is lactate important for gluconeogeneis s(structure)

A

lactate is very ismilar to pyrvate (same structure with 2 hydrogens added on)
therefore it can become pyruvate and then glucose

69
Q

if gluconeogenesis didnt happen, what would happen

A

we would have no way to maintain blood circulation levels without a food source therefore in periods of rest (like sleep) we would become hypoglycemic

70
Q

what is the reason the precursors to gluconeogenesis can easily turn into pyruvate

A

they are all 3 carbon based

71
Q

true or false: glycerol enters gluconeogenis at the same place as lactae and adenine

A

false, higher up

258: Physiology (25 decks)

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