Higher Human | Cellular Respiration

The following links offer some useful revision on Cell Structure to support your learning:

At Higher, you will need to know the following:

Glucose broken down, removal of hydrogen ions and electrons by dehydrogenase enzymes releasing ATP.
The metabolic pathways of cellular respiration are central to metabolism. They yield energy and are connected to many other pathways.
The role of ATP in the transfer of energy and the phosphorylation of molecules by ATP.
ATP is used to transfer energy to synthetic pathways and other cellular processes where energy is required.
Metabolic pathways of cellular respiration. The breakdown of glucose to pyruvate in the cytoplasm in glycolysis, and the progression pathways in the presence or absence of oxygen (fermentation).
The phosphorylation of intermediates in glycolysis in an energy investment phase and the direct generation of ATP in an energy pay-off stage. The role of the enzyme phosphofructokinase in this pathway.
The first phosphorylation leads to a product that can continue to a number of pathways and the second phosphorylation, catalysed by phosphofructokinase, is an irreversible reaction leading only to the glycolytic pathway. Pyruvate progresses to the citric acid cycle if oxygen is available.
The formation of citrate. Pyruvate is broken down to an acetyl group that combines with coenzyme A to be transferred to the citric acid cycle as acetyl coenzyme A. Acetyl (coenzyme A) combines with oxaloacetate to form citrate followed by the enzyme mediated steps of the cycle. This cycle results in the generation of ATP, the release of carbon dioxide and the regeneration of oxaloacetate in the matrix of the mitochondria.
Dehydrogenase enzymes remove hydrogen ions and electrons which are passed to the coenzymes NAD or FAD to form NADH or FADH2 in glycolysis and citric acid pathways. NADH and FADH2 release the high-energy electrons to the electron transport chain on the mitochondrial membrane and this results in the synthesis of the bulk of the ATP.
The electron transport chain as a collection of proteins attached to a membrane. NADH and FADH2 release the high-energy electrons to the electron transport chain where they pass along the chain, releasing energy. The energy is used to pump H ions across the inner mitochondrial membrane. The return flow of H ions drives ATP synthase and produces the bulk of the ATP generated by cellular respiration.
ATP synthesis — high energy electrons are used to pump hydrogen ions across a membrane and flow of these ions back through the membrane synthesises ATP using the membrane protein ATP synthase.
The return flow of these ions rotates part of the membrane protein ATP synthase, catalysing the synthesis of ATP.
The final electron acceptor is oxygen, which combines with hydrogen ions and electrons to form water.
Substrates for respiration. The role of starch, glycogen, other sugar molecules, amino acids and fats in the respiratory pathway.
Starch and glycogen are broken down to glucose for use as a respiratory substrate. Other sugar molecules can be converted to glucose or glycolysis intermediates for use as respiratory substrates.
Proteins can be broken down to amino acids and converted to intermediates of glycolysis and the citric acid cycle for use as respiratory substrates.
Fats can also be broken down to intermediates of glycolysis and the citric acid cycle
Regulation of the pathways of cellular respiration by feedback inhibition — regulation of ATP production, by inhibition of phosphofructokinase by ATP and citrate, synchronisation of rates of glycolysis and citric acid cycle.
The cell conserves its resources by only producing ATP when required.
The cell conserves its resources by only producing ATP when required. ATP supply increases with increasing rates of glycolysis and the citric acid cycle, and decreases when these pathways slow down. If the cell produces more ATP than it needs, the ATP inhibits the action of phosphofructokinase slowing the rate of glycolysis. The rates of glycolysis and the citric acid cycle are synchronised by the inhibition of phosphofructokinase by citrate. If citrate accumulates, glycolysis slows down and when citrate consumption increases glycolysis increases the supply of acetyl groups to the citric acid cycle.