L9- Kreb and ETC Flashcards
excess G-6-P can..
feed into the pentose phosphate pathway to produce NADPH for biosynthesis and 5C sugars
- stored as glycogen
both fructose and galactose can enter glycolysis via
some extra steps
which stage does kreb cycle begin
stage 3
at the end of glycolysis what are we left with
pyruvate (3C x 2)
what happens to pyruvate once it has been formed during glycolysis
is transported from cytoplasm across mitochondrial membrane into the matrix
which enzyme catalysis the combining of pyruvate + CoA +NAD+ to form Acetyl CoA
Pyruvate dehydrogenase (PDH)
pyruvate –> acetylCoA
3C to 2C
which cofactors does PDH require
FAD, thiamine pyrophosphate and lipoid acid- B-vitamins provide these factors
PDH catalysing pyruvate –> acetyl CoA is a ………. reaction
irreversible- releases CO2
–> key regulatory step
PDH is activated by
- Pyruvate
- NAD+
- ADP
- Insulin
- CoASH (coenzyme A- free SH group)
- Dephosphorylation
PDH is inhibited by
- Acetyl-CoA
- NADH
- ATP
- Citrate
- Phosphorylation
the TCA cycle is also known as
the kreb cycle
kreb cycle is considered the
hub of metabolism
- sugars
- fatty acids
- ketone bodies
- amino acids
- alcohol
where does the kreb cycle occur
in the mitochondrial matrix
acetyl converted to
2CO2–> by breaking C-C bonds in acetyl CoA
products of the kreb cycle
Glucose (6C) + 2 pyruvate (3C) + 2 acteyl CoA (2C) + TCA =
Products:
- 6NADH
- 2FAD2H
- 2GTP (ATP equivalent)
kreb cycle is
oxidative and releases some energy (GTP)
kreb cycle is regulate by
high and and low energy compounds (ATP/ADP and NADPH/NAD+ ratio)
4 main step of kreb cycle
- broken all C-C bonds
- oxidised all the C-atoms to CO2
- broken all the C-H bonds
- Transferred all the H atoms (H+ and e-) to NADH + H and FADH2
NADH and FADH produced in the kreb cycle are used to power
ATP synthesis in the ETC
what sort of reaction is the kreb cycle
substrate level phosphorylation
what is stage 4 of catabolism
the electron transport chain
what sort of reaction is the electron transport chain
oxidative phosphorylation
where does ETC occur
inner membrane of the mitochondria- cristae
during the ETC what happens to NADH and FADH2
re-oxidised–> to form more NAD+ and FAD+ which can be re-used
what is required during ETC
oxygen
- - Electrons transferred from NADH and FADH2 to molecular oxygen
two processes occur in ETC
- Electrons on NADH and FADH2 transferred through a series of carrier molecules to oxygens (Electron transport)
- Free energy released used to drive ATP synthesis (Oxidative phosphorylation)
describe how the ETC works
Electrons from NADH are passed onto an electron carrier PTC1, this drives Hydrogen atom from the matrix into the inner membrane.
• Electrons are transferred through a series of carrier molecules (mostly within proteins) to oxygen with release of energy
energy released during electrons transfer
1) 30% energy used to form proton gradient
2) the rest used to release heat
[H+] gradient across inner mitochondrial membraner
proton motive force
return of protons is
faired energetically by electrochemical potential
how do protons return from the inner membrane space to the mitochondrial matric
via ATP synthase
when H+ flows through ATP synthase down proton gradient
ATP synthesis
which reducing powerful has more energy : NADH or FAD2H
NADH
- NADH use 3 PTCs
- FADH2 uses 2 PTCs
- Greater PMF more ATP synthesised
when ATP is high and ADP what occurs to ATP synthase
no substrate to synthesise ATP –> inward flow of H_ stops
–> conc of H+ in intramitochondrial space increases preventing further H+ primping- stop ETC
example of ETC inhibitors
Cyanide and carbon monoxide
uncouplers
ETC and Cyanide and carbon monoxide
- Blocks electron transport e.g. prevents acceptance of electrons by oxygen
- No oxidative phos- no ATP
ETC and uncouplers
- Increase permeability of the mitochondrial inner membrane to protons
- Decreases proton gradient and therefore reducing proton motive force
- No phosphorylation of ADP by ATP synthase
Ox/Phos diseases
Genetic defects in proteins encoded by mtDNA (some subunits of the PTCs and ATP synthase) decrease in ETC and ATP synthesis .
brown adipose tissues contains a high conc of
thermogenin
thermogenin
a UCP1 (uncoupling protein) –> naturally occurring uncoupling protein
brown adipose tissue and its response to the cold
noradrenaline (norepinephrine) activates :
- Lipase which releases fatty acids from Triacylglycerol
- Fatty acid oxidation NADH/FADH2 electron transport
- Fatty acids activate UCP1
- UCP1 transports H+ back into mitochondria
- So, Electron Transport uncoupled from ATP Synthesis.
- Energy of p.m.f. is then released as extra heat.
family of UCPs
role in heat generation by uncoupling- may have other functions
who has more brown adipose tissue
newborn infants and hibernating animals
newborn infants
have lots of brown adipose around vital organs to maintain heat
oxidative phosphorylation
- requires membrane associated complexes e.,g. inner mito membrane
- cannot occur in absence of oxygen
- major process for ATP synthesis in cells requiring large amount of energy
substrate level phosphorylation
- requires soluble enzymes
- can occur in absence of O2
- minor process for ATP synthesis inc ells requiring large amounts of energy
summary of ATP synthesis from glucose
glucose –> pyruvate –> 6CO2 and 6H20 + 32 ATP
