The Krebs Cycle and Oxidative Metabolism Flashcards
where does the Krebs Cycle / The Citric Acid Cycle occur?
what 2 things do we need to start TCA?
what is TCA depedent on?
- Krebs cycle: @ mitochondria
- starting point: Acetyl Co-A & oxaloacetate
- TCA dependent on oxygen presence !
what happens (overview) to acetyl co-A during the TCA?
Acetyl CoA combines with oxaloacetate to form Citrate.
(Citrate is a tricarboxylic acid, hence the name TCA)
This enters the cycle and is progressively oxidised, each time producing NADH/FADH2, until finally forms oxaloacetate again and the cycle can begin again.
Acetyl Co-A is one of the starting molecules needed for TCA. But what is the equation for the formation of Acetyl Co-A from pyruvate?
what is the enzyme used to catalyse this reaction?
what nutrition is needed for this reaction?
- pyruvate + CoA + NAD+ –> acetyl Co-A + Co2 + NADH
- enzyme: pyruvate dehydrogenase (PDH)
- co-enzymes are members of the B-vitamin family. uses TPP (aka vitamin B1)
why is pyruvate dehydrogenase complex (PDH) a pivatol enzyme?
why does PDH need to be regulated?
when is PDH blocked? (2)
pyruvate dehydrogenase is key because it determines whether acetyl Co-A (made from pyruvate) will enter the TCA / Krebs cycle
- PDH needs to be regulated to make sure there is enough ATP for the cell
- PDC is blocked when
a) **levels of Acetyl CoA levels are high
b) ** If reduced NAD levels are high (
- When blood glucose is high, PDC is more or less active?
- When blood glucose is low, PDC is more or less active?
- When blood glucose is high, PDC is more active
- When blood glucose is low, turn down PDC (reducing energy production from glucose)
PDH is regulated in two ways:
- PDH is de/-phosphorylated by which enzymes? what do they add / remove? what is their effect?
which substances control 1.?
:)
- PDH **Kinases inhibit PDH by adding PO4
- PDH PhosphatasesactivatePDHbyremoving**PO4
//
- *control of PDH kinases**
- PDH kinases are activated by ATP, acetyl Co-A and NADH (last two are products of PDH) = switch off PDH.
- Pyruvate & insulin inhibits PDH Kinasese (as pyruvate wants PDH to be active to break pyruvate down) = switch on PDH.
- *control of PDH phosphatases**
- Ca2+ ions activate PDH phosphatises - increases PDH. occurs in muscle -> eventually get more ATP production = switch on PDH
- insulin activates PDH phosphatases - actives PDH
to put simply - insulin has what effect on PDH?
what effect does insulin have of kinases & phosphatases?
what do adrenaline and glucagon do to PDH? - why?
insulin caueses the activation of PDH & eventual production of acetyl co-A
insulin = -ve effect on kinases (which inhibit PDH)
+ve effect on phosphatases (which activate PDH)
adrenaline and glucagon: want pyruvate untouched, so it can be used to make glucose via gluconeogenesis = inhibit PDH
* acetyl co-A is the input for TCA. acetyl co-A can be produced by three ways. What are they? *
1.Glycolysis of glucose to pyruvate
•Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)
•Produces 2 reduced NAD molecules per glucose
•1 reduced NAD per pyruvate
2.Transamination of glucogenic amino acids to pyruvate
• Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)
3.Beta-oxidation of fatty acids directly to acetyl-CoA
•Produces 1 NADH and 1 FADH2 per acetyl-CoA
so after acetyl Co-A is formed. it feeds into the TCA cycle,
where dose the TCA cycle occur?
(where does the electron transport chain occur - later on but still good to know!)
how many acetly Co-A enter the TCA (from one glucose molecule)
what are the end products of TCA cycle? (3)
- TCA cycle occurs in the mitochondrial matrix
- ETC occurs in the inner membrane of the mitochondria
- acetyl Co-A: 2 molecules made / go into the TCA from only one molecule glucose
- TCA end products:
a) 1 GTP / ATP
b) 3 NADH
c) 1 FADH
BUT BECAUSE HAVE 2 ACETLY CO-As GOING INTO TCA:
a) 2 GTP / ATP
b) 6 NADH
c) 2 FADH
what else can be added to the krebs cycle (apart from acetyl co-A and oxaoloacetate)
intermediates in the krebs cycle can be added from the degradation of amino acids
what are the reduced electron carriers that feed into the ECT from the TCA?
3 NADH + 1FADH2
give overview of ETC :)
where does it occur?
- location: inner membrane of matrix
- reduced co-enzymes NADH & FADH used to create a proton gradient across the inner membrane of the mt
- NADH & FADH offload their H+ to proton complexes
- H+ passes from one complex to another (1->4) in a series of REDOX reactions
- As H+ passes from complex to another in REDOX reactions, the energy produced is sufficient to pump protons from the inner maxtrix, across the inner mt membrane, into the inner membrane space
- this creates a proton gradient. protons can only return to the matrix via ATP synthase -> where ATP is produced
ETC:
what happens at complexes 1-4 ?
@ which complexes are protons from transferred from the matrix to the intermembrane space, making a proton gradient?
- *Complex 1
- ** NADH –> NAD+ + H.
- H+ is transfered to ubiqunione (electron carrier)
- *Complex 2**
- FADH –> FAD + H+
- H+ transfers electrons to ubiqunione
Complex 3
transfers electrons from ubiqunione to cytochrome C
- *4th protein complex
- electrons frocytochrome Ctransferred to 1/2 O2 moleculeis the final electron acceptor from electron transport chain. h20 is produced.**
- protons pumped at complexes 1, 3 & 4 = proton gradient
* why do we need o2 for ETC to occur? *
what happens if we dont have any O2?
- @ 4th protein complex, 1/2 O2 molecule is the final electron acceptor from electron transport chain
- without O2:
- NO ATP Produced
- electrons get stuck on chain. stops the redox reactions = no protons pumped across = no proton gradient = no ATP !
how is ATP produced at end of the ETC?
- protons flow back to matrix through ATP synthase. This drives phosphorylation of ADP:
ATP produced **by oxidative phosphorylation:
ADP + P –> ATP**
