Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIOL301 > BIOL301 class 14 > Flashcards

BIOL301 class 14 Flashcards

1
Q

oxidative phosphorylation

A

converting the electrons captured from fuel oxidation into ATP, powered by a proton motive force generated by a series of coupled reductions/oxidations
- mitochondrial inner membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

mitochondrial topology

A

outer membrane: freely permeable to small molecules and ions
inner membrane: impermeable to most small molecules and ions including H+ & contains respiratory electron carriers (complexes I-IV), ADP-ATP translocase, ATP synthase (F0,F1), and other membrane transporters
matrix: contains pyruvate dehydrogenase complex, citric acid cycle enzymes, fatty acid beta oxidation enzymes, and amino acid oxidation enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Electron Transport Chain

A
  • part solid state wiring, part diffusable electric grid
  • electrons flow toward increasing reduction potential
  • increasing standard reduction as it goes from complex I-IV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why does FADH2 from the TCA cycle generate fewer ATP molecules than NADH?

A
  • NADH produces more ATP bc it contributes more to the energy making process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Malate-Aspartate Shuttle: “Transport” of Glycolysis NADH’s

A

Problem: The inner membrane is impermeable to NADH
- NADH from glycolysis (cytosol) gets into the mitochondrial matrix through shuttles
- not a problem for NADHs produced from the TCA cycle bc the TCA cycle already happens in the mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what type of transporter is the malate-alpha-ketogluterate transporter?

A
  • ANTI
  • for every malate coming in, you have to kick an alpha keto gluterate out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what type of transporter is the glutamate-aspartate transporter?

A
  • ANTI
  • for every aspartate coming in, you have to kick a glutamate out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what CAN go through the membrane?

A

malate <–> alpha-ketoglutarate via antiporter
aspartate <–> glutamate via antiporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what CANNOT go through the membrane?

A

NADH (you need to reduce oxaloacetate to malate)
Oxaloacetate (need to transform into aspartate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

another path for glycolytic NADH’s to move electrons into the mitochondria

A

the glycerol phosphate shuttle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Complex I

A

NADH + H+ –> NAD+
4H+ coming out for every NADH that is oxidized
- reduced NAD+ (NADH) provides electrons (reducing power) to the ETC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what problems might riboflavin deficiency cause?

A

anemia , low energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the relative reduction potentials for NADH vs FMN? Which is the stronger oxidant?

A

NADH: - 0.32 V
FMN : - 0.219 V
- higher reduction potential = stronger oxidizing agent
- stronger oxidizing agent = more likely to accept electrons and undergo reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complex I

A

Ubiquinone Oxidoreductase
1) NADH hydride ion reduces FMN, which then hands off 2 electrons through Fe-S centers, ultimately reducing Q (ubiquinone) to QH2 (Ubiquinol)
2) The transfer of 2 electrons drives the expulsion of 4 protons from the matrix into the intermembrane space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fe-S centers

A
  • grabs and hands off electrons within complexes
  • single electron transfers through Fe atoms
  • different arrangements affect the reduction potentials of the Fe’s in the different Fe-S centers, allowing for electron flow toward the reduction of Q
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mobile Component of the ETC “wire” I

A

Coenzyme Q
- 1 e- reduces uniquinone (Q) to semiquinone (‘QH)
- 2 e-‘s from NADH or FADH2 reduce ubiquinone to ubiquinol (Q-QH2)

17
Q

ubiquiNONE (Q)

A

fully oxidized (no Hs)

18
Q

semiquinone radical (‘QH)

A

intermediate, not fully happy yet

19
Q

ubiquiNOL (QH2)

A

fully reduced (Hs)

20
Q

would coenzyme Q be more comfortable in aqueous or lipid/hydrophobic environments?

A

hydrophobic environments

21
Q

Complex II

A

Succinate Dehydrogenase
- the only membrane-bound enzyme in the TCA cycle
- has nothing to do with complex I
- goes directly to Q
- no H+ are ejected by this complex
1) oxidation of succinate to fumerate in TCA cycle reduces FAD –> FADH2
2) Oxidation of FADH2 –> FAD then moves 2 electrons through Fe-S oxidoreduction “wire” to reduce Q –> QH2
3) QH2 is then released into the bilayer

22
Q

what does “P side” and “N side” of the membrane refer to?

A
  • The P side of the membrane refers to the intermembrane space (positive side)
  • the N side of the membrane refers to the matrix (negative side)
23
Q

multiple paths bring in electrons to Q in ETC

A

picture

24
Q

“Fixed” (non-motile) cytochromes in the ETC

A

have hemes with different structures and interactions with proteins that influence the reduction potentials of the iron atom

25
Q

Complex III

A

Ubiquinone: Cytochrome c Oxidoreductase
- a problem arises here with electron accounting: Reduced Q (QH2) is carrying 2 electrons, but cytochrome C can only accept one electron
- two single electron transfers are required to fully oxidize QH2 –> Q ( 2 separate electron transfers from Q –> Cytochrome C)

26
Q

Mobile component of the ETC “wire” II: Cytochrome C

A
  • Cytochrome C is a very small protein with a heme in the middle that allows it to accept electrons
27
Q

would you predict cytochrome C to be comfortable in aqueous environments?

A

yes

28
Q

complex IV: Cytochrome Oxidase

A

1) in total, 4 sequential electrons from 4 cytochrome c’s + 4 protons from the matrix reduce O2 -> H2O
- 4 more protons are pumped out of the matrix
2) since single e-‘s are transferred, O2 reduction intermediates (H2O2 and OH-) are presumed to be held until full reduction is complete

29
Q

the ETC is a source of oxygen radicals

A
  • Electron influx and oxygen reduction must be matched to prevent formation of Reactive Oxygen Species (ROS)
  • If O2 encounters reduced Q, O2 is easily reduced to form a superoxide radical ( because QH2 carries high-energy electrons that oxygen really wants)
30
Q

Reactice Oxygen Species (ROS)

A
  • highly reactive, damaging molecules
  • ROS scavenging pathways can prevent excessive accumulation
  • Damage can accumulate (aging)
  • this can also be harnessed for defenses against invaders (innate immune system)
31
Q

what happens to ROS that end up in the cytoplasm?

A

ROS that reach the cytoplasm are harmful to cells. To protect themselves, cells have natural defenses like enzymes and molecules that neutralize ROS, repair damaged parts, and remove them. This helps keep the cells healthy and functioning properly.

32
Q

how is electrochemical potential from proton gradient couples to ATP synthesis?

A

The electrochemical potential created by the proton gradient across the inner mitochondrial membrane powers ATP synthesis through a protein called ATP synthase. As protons flow through ATP synthase, it spins like a tiny turbine, converting the energy into ATP. This process efficiently produces ATP, the cell’s main energy source.

33
Q

ATP Synthesis

A
  • clockwise rotation
  • influx of H+ through F0 subunit drives ATP synthesis
34
Q

ATP Hydrolysis

A
  • anticlockwise rotation
  • ATP hydrolysis via F1 catalytic subunits can drive H+ accumulation
35
Q

Model of ATP Synthesis

A

1) Open (can exchange ATP for ADP + Pi)
2) Loose (coupling of ADP + Pi are brought in proximity)
3) Tight (ADP + Pi are forced together to make ATP)

36
Q

Toxins and man-made poisons designed to interfere with ATP Synthesis

A

uncoupling of phosphorylation from electron transfer
- FCCP
- DNP
- Valinomycin
- thermogenin

37
Q

Proton gradient disruptors (uncouplers) speed up the ETC and produce Thermal energy instead of ATP

Why would uncoupling of the ETC from ATP synthesis SPEED UP the ETC?

A

uncoupling the ETC from ATP synthesis allows electron transport to proceed at a faster rate because there is no feedback inhibition from ATP production. This can have physiological implications, such as increased heat production in certain tissues or enhanced metabolic activity in cells.

38
Q

OX-PHOS Uncoupler: 2,4-Dinitrophenol (DNP)

A
  • marketed as diet pills on the internet
    DNP causes the body to burn more calories and fat by increasing metabolism and generating heat. This can lead to weight loss.
  • high body temperature
  • elevated heart rate
  • a lot of sweating
  • elevated breathing rate
39
Q

Thermogenin (aka uncoupling protein 1) UCP1

A
  • found in brown fat (in infants and hibernating animals); white fat is for energy storage; brown fat is for heat production
  • Its job is to generate heat by making mitochondria produce heat instead of energy. This helps keep the body warm, especially in cold weather.

BIOL301 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions