cell integrity Flashcards
- Why does re-oxidation of FADH2 mean that less ATP is produced compared to oxidation of NADH?
Because Complex I is bypassed, so fewer H+ are pumped into Intermembrane space, so less ATP is produced
- What does it mean if a redox couple has a negative redox potential?
Redox couple has a tendency to donate electrons, so it has more of a reducing power than hydrogen
- What are the two parts of ATP Synthase called?
- How does ATP Synthase allow the production of ATP?
F0 is part bound to membrane
F1 is part suspended in matrix
H+ moves from the intermembranal space to the matrix
as a result, f0 rotates and absorbs this potential energy
causing F1 to synthesise ATP
- Why does ATP production vary in the ATP Synthase?
Rotation of enzyme drives the transitional states with altering affinities for ATP and ADP
The directional flow of protons through ATP Synthase decides whether ATP synthesis or hydrolysis occurs If there is a higher concentration of H+ in intermembrane space and lower concentration of ATP in matrix, then the conditions are more favourable towards ATP Synthesis
- How can we use the Oxygen Electrode to measure changes in ETC?
- what is the structure of an oxygen electrode?
By placing suspension of mitochondria into chamber, we can see effects of various substrates and inhibitors on ETC through changes in [O2]
teflon membrane is base of chamber- oxygen permeable
above membrane is two electrodes- platinum cathode and silver anode
oxygen diffuses through teflon membrane and reduced to water at platinum cathode
ag is oxidised to AgCl due to KCL electrolyte
resulting current is proportional to oxygen conc in chmaber
- How does rotenone reduce oxygen consumption in the electron transport chain?
It inhibits electron transfer from Complex I to Coenzyme Q
which also inhibits production of NADH by citrate metabolism and ultimately oxygen consumption
but ultimately only slows electron transport as a whole because complex 2 can still be used
- How does Complex II reduce the effects of rotonone?
Complex II passes electrons directly from FADH2 to Coenzyme Q
This bypasses Complex I and therefore the effects of rotonone
- How do CN- and N3- act as metabolic poisons?
They bind with high affinity to Fe3+ form of haem group
in cytochrome oxidase complex (IV)
blocking final step of ETC
- How does Malonate act as a metabolic poison?
Resembles succinate and acts as competitive inhibitor of succinate dehydrogenase (complex II)
inhibiting oxidation of succinate to fumarate
slowing the flow of electrons from succinate to ubiquinone
- How does Oligomycin act as a metabolic poison?
It is an antibiotic produced by Streptomyces that inhibits oxidative phosphorylation by binding to F0 of ATP Synthase and blocking the flow of H+ through the enzyme
- How does DNP induce weight loss?
By transporting protons across the mitochondrial membrane
Thereby uncoupling oxidative phosphorylation from ATP production markedly increasing the metabolic rate and body temperature This is because of the compensatory effect to increase metabolic rate to produce the energy needed to maintain the body
energy used to pump H+ dissipates as heat hence inc body temp
- Why did people taking DNP die?
- How does substrate level phosphorylation differ from oxidative phosphorylation?
The margin between the slimming dose and that required to poison or kill is slight
Oxidative phosphorylation ultilises an electron transport chain to drive ATP production
substrate level phosphorylation is the direct transfer of high energy phosphate to ADP
- Explain as to how the electron transport chain works?
NADH comes from cytoplasm through malate-aspartate shuttle and FADH2 comes from cytoplasm through glycerol-3-phosphate shuttle
NADH donates electron to complex I → NAD+ and a H+ FADH2 donates electron to complex II- another proton released Electrons from either complex flow into coenzyme Q which passes electrons to complex III Complex III uses its cytochromes to pass the electrons to cytochrome C which then transports these to complex IV Complex IV then gives electrons to Oxygen to make it electronegative enough to bind to hydrogen which forms water At same time as transporting electrons energy is released and so Complexes I, III and IV transport H+ from matrix to IMS
This creates an electrochemical gradient, as there is now a higher conc of H+ in the IMS than in matrix and so H+ is transported by a membrane transporter protein called F0 which is bound to F1 (ATP synthase)
As a H+ passes through the F0 into the matrix, ATP is synthesised
where does oxidative phosphorylation take place?
where does krebs cycle take place
inner membrane
mitochondrial matrix
what is respiratory control?
uptake of oxygen is controlled by the components of ATP synthesis (ADP and phosphate)
allows body to adapt oxygen consumption to energy requirements
