Oxidative Phosphorylation
Citric Acid Cycle Steps
Page 1: Isomerization
Step 2: Citrate isomerized to Isocitrate by aconitase.
Involves a dehydration and subsequent rehydration.
Tertiary alcohols cannot oxidize without breaking carbon-carbon bonds, necessitating isomerization to generate a secondary alcohol (Isocitrate).
Oxidation of Isocitrate
Step 3: Oxidation of Isocitrate to α-Ketoglutarate by isocitrate dehydrogenase.
Results in loss of CO2 and reduces NAD+ (or NADP+) to NADH (or NADPH).
Oxidation of α-Ketoglutarate
Oxidation of α-Ketoglutarate to Succinyl-CoA by α-ketoglutarate dehydrogenase complex.
Results in loss of CO2 and reduces NAD+ to NADH.
Similar to the reaction converting pyruvate to acetyl-CoA, utilizing the same cofactors (TPP, lipoic acid, FADH) as the PDH complex.
Conversion to Succinate
Conversion of Succinyl-CoA to Succinate by succinyl-CoA synthetase.
Regenerates Coenzyme A and forms either ATP or GTP via substrate-level phosphorylation.
Oxidation to Fumarate
Oxidation of Succinate to Fumarate by succinate dehydrogenase.
Reduces one FAD to FADH2.
Succinate dehydrogenase exists tightly bound to the inner mitochondrial membrane.
Hydration to Malate
Hydration of Fumarate to Malate by fumarase.
Requires a water molecule for hydration.
Oxidation of Malate
Oxidation of Malate to Oxaloacetate by malate dehydrogenase.
Converts NAD+ into NADH.
Energetically unfavorable but driven forward by the next reaction, maintaining low oxaloacetate levels.
Summary of Citric Acid Cycle Outputs
Outputs:
Acetyl-CoA leads to: Citrate → Isocitrate → α-Ketoglutarate → Succinyl-CoA → Succinate → Fumarate → Malate → Oxaloacetate.
Produces NADH, FADH2, CO2, and GTP (ATP).
Amphibolic Nature of Citric Acid Cycle
Anabolic and Catabolic Functions
The citric acid cycle is amphibolic, serving both anabolic and catabolic purposes.
Compounds from the cycle can be siphoned off for use in other metabolic pathways.
Regulation of Cycle
Key Regulators
Important molecules: Pyruvate, ATP, Acetyl-CoA, NADH, ADP, Ca2+.
Regulation involves various key enzymes:
Citrate synthase, isocitrate dehydrogenase, and α-ketoglutarate dehydrogenase are all influenced by the concentrations of their product/reactants and energy status.
Oxidative Phosphorylation
Purpose of Reduced Carriers
Reduced NADH and FADH2 are generated in glycolysis and the citric acid cycle.
High-energy electrons in these carriers are passed along the mitochondrial electron transport chain, generating ATP.
The final electron acceptor is O2.
Mechanism
High-energy electrons in NADH and FADH2 are transferred through the mitochondrial inner membrane's electron transport chain.
Electrons lose energy (standard reduction potential, Eo’) as they are passed along.
NADH and FADH2 enter the chain from different pathways, converging at Coenzyme Q.
Final Electron Transfer
Complex IV transfers electrons from Cyt c to O2 via cytochromes.
Reaction: 4 cyt c (Fe+2) + O2 + 8H+ → 4 cyt c (Fe+3) + 4H+ + 2 H2O.
The transfer involves the pumping of protons across the mitochondrial membrane.
Inhibition and Gibbs Free Energy
Inhibition of Electron Transport
Various compounds can inhibit electron transport, which can serve as tools to determine carriers' order in the chain.
ΔGo’ Calculations
Energy considerations for ATP synthesis:
Two distinct activities:
Electron flow from NADH to O2 (ΔGo’ = -220 kJ/mol)
Phosphorylation of ADP to form ATP (ΔGo’ = +31 kJ/mol).
Mechanism of ATP Synthesis
Chemiosmotic coupling drives ATP synthesis.
Protons are pumped into the intermembrane space, generating a gradient.
ATP synthase harnesses this gradient to produce ATP via proton passage.
Final Notes
Yield from Glucose
Final balance for one glucose molecule:
Assigns 2.5 ATP/NADH and 1.5 ATP/FADH2, yielding approximately 31 ATP per glucose.
ΔGo’ for glucose oxidation: -2870 kJ/mol, with ATP hydrolysis being -30.5 kJ/mol, leading to an efficiency of conversion to ATP of about 32%.