Flashcards in TCA Cycle and ETC Deck (16):
What is the function of the pyruvate dehydrogenase complex?
Converts pyruvate to acetyl CoA at the end of glycolysis
What are the most important products of the TCA cycle for ATP production?
How many 'steps' are there in the PDC?
Name a cofactor that is used by PDC and an example of it's source
thiamine pyrophosphate (TPP) from vitamin B1
How many complexes is the ETC comprised of?
Describe what happens at complex I
NADH converted to ubiquinone
Describe what happens at complex II
FADH converted to ubiquinone
Describe what happens at complex III
Ubiquinone converted to cytochrome C
Describe what happens at complex IV
Cytochrome C to oxygen
Give a reason as to why ATP wouldn't be produced from the ETC
If there charge (electrochemical/proton gradient) is neutralised or if there is another way for protons to pass across the membrane other than through ATP synthase
How do 'natural antibiotics' work?
They affect coupling reactions (alter the movement of protons across the membrane to release ATP) in bacteria.
How is PDC regulated?
Feedback inhibition and cavalent modification through phosphorylation y both PDH kinase and protein kinase A
How is the TCA cycle controlled?
Rate depends upon NAD+ availability so is essentially substrate controlled as well as linked to ATP:ADP ratio as NAD+ availability is dependent on rate of ETC
What metabolic adaptations occur in hypoxia?
Limit ATP use by switching off non-essential cell functions, improve anaerobic ATP production efficiency and limit oxidative stress by preventing entry to mitchondria (preventing TCA and ETC)
How are metabolic adaptations to hypoxia mediated via HIF1?
Can be mediated via changes to gene expression. In normoxia HIF1a subunit degraded where sin hypoxia it is stabilised and binds to upstream elements of promoters and causes the down-regulation of mitcohondrial respiration as well as promoting loss of mitochondria (to prevent risk of oxidative stress and ischaemia)