Fundamentals of the Living Cell
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What do competitive inhibitors do and give an example of one
They have a similar shape to the enzyme’s substrate and bind to the enzymes active site blocking the substrate from binding. e.g , Statins(limits cholesterol synthesis)
What do non-competitive inhibitors do and give an example of one
binds to an allosteric site and changes the enzyme’s shape so substrate can no longer bind to the enzymes active site
what happens the the Vmax(fastest possible rate of an enzyme-catalysed reaction) and Km (substrate affinity) in competitive inhibitors
Vmax stays the same Km increases
what happens the the Vmax and Km in non-competitive inhibitors
Vmax decreases Km stays the same
what enzymes convert glucose into Glucose-6-phosphate(G6P) and what else is used
Hexokinase - muscle Glucokinase - liver 1 ATP molecule is metabolised
What does G6P convert into
Fructose-6-phosphate(F6P)
What is used to convert F6P into F1,6P
1 ATP is metabolised Phosphofructokinase
What 3 carbon molecules are F1,6P broken down into and which one directly continues glycolysis
Dihydroxyacetone phosphate(DHAP) and Glycealaldehyde-3-phosphate (G3P) and G3P continues glycolysis so there are now 2 G3P
What is used to turn one G3P molecule into Phosphoenol pyruvate
1 NAD+ is reduced to NADH 1 Pi is used 1 ATP is synthesised
What is used to turn Phosphoenol pyruvate into pyruvate
1 ATP is synthesised
How is Glycolysis regulated
By regulating the enzymes
How do we regulate Hexokinase/Glucokinase, Phosphofructokinase and Pyruvate kinase
Hexokinase - inhibited by G6P Glucokinase - Induced by insulin Phosphofructokinase - inhibited by ATP and activated by AMP/ADP Pyruvate kinase - inhibited by ATP and activated by F1,6P
What is the only way pyruvate can enter the mitochondria and why
In aerobic conditions (presence of O2) otherwise pyruvate will convert into lactic acid
How does pyruvate convert into Acetyl CoA
NAD+ is reduced CO2 is lost Coenzyme A is added
What enzyme catalyses the conversion of pyruvate into Acetyl CoA
Pyruvate Dehydrogenase (PDH)
How is Pyruvate Dehydrogenase (PDH) regulated
Inhibited by NADH and Acetyl CoA Phosphorylation by a kinase and phosphatase
What is the main purpose of the Krebs (Citric Acid) Cycle?
The Krebs cycle oxidizes acetyl-CoA into CO₂, generating NADH and FADH₂ to power ATP production in the electron transport chain
What are the major steps of the Krebs cycle?
Acetyl-CoA + Oxaloacetate → Citrate (citrate synthase) Citrate → Isocitrate Isocitrate → α-Ketoglutarate (NADH + CO₂) α-Ketoglutarate → Succinyl-CoA (NADH + CO₂) Succinyl-CoA → Succinate (GTP/ATP) Succinate → Fumarate (FADH₂) Fumarate → Malate Malate → Oxaloacetate (NADH) Oxaloacetate is regenerated so the cycle can continue.
What is produced from one turn of the Krebs cycle (per acetyl-CoA)?
3 NADH * 1 FADH₂ * 1 GTP (≈1 ATP) * 2 CO₂
What happens to NADH and FADH2 in the ETC
They lose electrons NADH loses to enzyme complex 1 and FADH2 to enzyme complex 2
where do these electrons move to lower the energy levels
Coenzyme Q
Where are protons pumped
intermembrane space
What molecule acts as the final electron acceptor
O2
During chemiosmosis what enzyme is used to join ADP and Pi to form ATP
ATP synthase