Chapter 3 Study Questions (Part 5) Flashcards
how does the lack of oxygen affect ETC? why?
can’t oxidize the last two transporters. shuts down.
how does the lack of oxygen affect chemiosmosis? why?
shuts down.
how does the lack of oxygen affect the TCA cycle?
shuts down. no pyruvate means FADH2 and NADH depleted, means no acetyl CoA, means can’t be oxidized.
how does lack of oxygen affect glycolysis and why?
nothing happens. it’s unaffected because glycolysis doesn’t use O2.
why does pyruvate build up in cells under anaerobic conditions?
not converted to acetyl, gets reduced to lactate instead.
what is the role of lactic acid fermentation?
regenerate NAD to keep glycolysis going. lactate is byproduct of it, that’s it.
when would we want to regenerate NAD+ ?
to run glycolysis under low oxygen conditions
describe the effect of regenerating NAD+ on O2 and CO2 levels
no O2 required, no CO2 produced
when tissue gets reoxygenated, what happens first?
ETC –> chemiosmosis –> oxidative phosphorylation
when tissue gets reoxygenated, what happens to NADH and FADH2?
they get oxidized
when tissue gets reoxygenated, what happens second?
TCA
when tissue gets reoxygenated, what happens to pyruvate levels and why?
you get back the pyruvate you lost earlier. it’s a reversible reaction taking place due to the law of mass action.
why is the amount of ATP produced from NADH made in glycolysis not always the same?
what happens after Fructose-1,6-Bisphosphate is made?
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
what does FADH2 do with its 2e-?
passes them to coenzyme Q in the inner mitochondrial membrane.
where is coenzyme Q located? why is that significant?
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
what happens to the e- that get unloaded at stage 2 of the ETC? why is that significant?
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
which pathway of cellular respiration produces ATP the quickest?
glycolysis
which pathway of cellular respiration produces the most ATP?
oxidative phosphorylation
why is it said that triglycerides are guilt for energy storage?
what are the different sources for gluconeogenesis?
1 is glycogen, glycerol.
minor: glycerol, lactate.
starvation conditions: protein.
why can’t arbon from fatty acids be used to make glucose in gluconeogenesis?
carbons are lost as CO2
why can’t acetyl CoA made from pyruvate be used to make glucose?
large NEGATIVE delta G aka not reversible!
how can a protein be used to make glucose?
by recycling amino acid intermediates into the TCA cycle to make glucose
what hormone is released in response to low blood glucose?
glucagon
why do we need to maintain blood glucose levels?
body prefers glucose as energy source. especially brain. RBCs only do glycolysis
what is B-oxidation?
B carbon is oxidized by exchanging the H for a doubled bond O
why does excessive B-oxidation lead to keton body formation?
CoA removes one 2C acetyl group and leaves behind a new COOH end
why does excessive B-oxidation lead to ketone body formation?
CoA removes one 2C acetyl group and leaves behind a new COOH end
why is excessive ketone body formation potentially dangerous?
super acidic, can be lethal. overwhelms TCA and can’t go backwards.
what energy soure can be used to make acetyl CoA to feed the TCA cycle?
at the beginning: glucose and fatty acids
in the middle: glucose, fatty acids, protein
what is the warburg effect?
accelerated glycolytic pathway. the activity of major enzymes is accelerated.
what are the three major enzymes involved in the glycolytic pathway?
PFK
pyruvate kinase
hexokinase
what effect would a compound that inhibits PFK have on tumor growth and why?
limit PFK, limit speeding up back half
what effect would a compound that inhibits pyruvate kinase have on tumor growth and why?
it’s like reverse mass action: slows down back half
what does phosphofructokinase do?
rate determining step, mass action, commits glucose
what does pyruvate kinase do?
intermediate of the front half speeds up the back half
