whats the role of NADH + FADH in etc
NADH + FADH deliver high -energy elctrons to the ETC
NADH donates to complex 1
FADH donates to complex 2
where is ETC / oxidative phosphorylation
inner mitochondrial membrane
proton pumps
electrons flow down ETC, energy released is used to pump H+ ions
from matrix to intermembrane space creating steep proton electrochemical gradient
chemoisosmosis
H+ diffuse back into matrix via ATP synthase
this drives oxidative phosphorylation
ADP+Pi - ATP
oxygen
final electron acceptor
accepts -
electrons from ETC
protons from H+
forms water
what happens if no O2
ETC stops, no proton gradient, no ATP, cell dies
why is cynaide lethal
inhibits the FINAL carrier in the ETC (Cytochrome Oxidase). This stops electrons from ever reaching Oxygen. The entire chain backs up immediately like a massive traffic jam. No ATP can be made at all.
why is barbiturates not lethal
These usually inhibit an EARLY carrier (Complex I). While this stops Reduced NAD from working, Reduced FAD can still join the chain further down at Complex II. You make much less ATP, but you make some.
What are the components of the ETC?
A series of protein complexes (electron carriers) and coenzymes embedded in the membrane, plus the enzyme ATP Synthase
How do Reduced NAD and Reduced FAD start the process?
They are oxidized. They deliver Hydrogen atoms which split into:
High-energy electrons - Go into the chain.
Protons - Go into the mitochondrial matrix solution.
What happens as electrons move through the carriers?
series of Redox reactions. As electrons move from a high energy level to a lower one, they release energy.
How is ATP actually made here?
The flow of protons through ATP Synthase provides the energy to drive the oxidative phosphorylation
ADP + Pi = ATP
