Metabolic Poisons Flashcards
Explain the coupling of the electron transport chain and oxidative phosphorylation. What does this ensure?
As substrates move along the ETC, each component uses the energy released in the electron transfer to transport one H+ across the inner mitochondrial membrane.
The H+ concentration is therefore higher on the outer side of the membrane.
The electrochemical gradient creates a temporary store of energy that is used by ATP synthase to phosphorylate ADP to ATP. The H+ flow back across the membrane.
This ensures that substrates are only metabolised when there is need for ATP.
Why is the rate of respiration higher in the presence of succinate and ADP than with glutamate, malate and ADP?
Glutamate and malate are NADH-linked substances. These feed electrons into the ETC via NADH dehydrogenase (complex 1) and so form 3ATP for each oxygen atom reduced to H2O.
Oxidation of succinate feeds electrons into the ETC via FADH2 and succinate dehydrogenase (complex 2). Only 2 ATP are generated per oxygen atom that is reduced.
To generate the same amount of ATP, more succinate needs to be oxidised.
Why most glutamate and malate be added together?
They are both required for the malate-aspartate shuttle.
Oxaloacetate concentration is normally very low in mitochondria. Addition of malate alone causes oxaloacetate build up.
This would inhibit malate dehydrogenase therefore inhibiting NADH production.
Addition of glutamate allows the excessive oxaloacetate to be removed from the mitochondrial matrix via the malate-aspartate shuttle.
What happens to respiration when KCN is added?
KCN reacts covalently with Fe3+ in cytochrome oxidase.
This inhibits the terminal step in the ETC.
Respiration ceases.
Under normal circumstances, what would happen to respiration after addition of oligomycin?
Oligomycin interferes with and reduces the ability of ATP synthase to utilise the H+ electrochemical gradient.
Inhibits respiration.
What does DNOC poisoning do? Why does it increase body temperature and and respiratory rate?
DNOC uncouples the mitochondria. The Kreb’s Cycle and oxidative phosphorylation work maximally but the link to ATP synthesis is broken.
DNOC and aromatic weak acids pass across the mitochondrial inner membrane in their undissociated form and so dissipate the electrochemical gradient (form DNOC-H).
The potential energy is released as heat.
The respiration rate increases to try to produce more ATP.
Why does DNOC poisoning cause absence of body fat?
Fatty acids from the triglycerides stored in adipose tissues is used as a fuel in the uncontrolled respiration.
Why does DNOC poisoning cause rapid rigor mortis?
There is a very low ATP concentration. There is no ATP to displace ADP on the myosin heads to allow dissociation from the myosin binding site.
What effect does DNOC poisoning cause on the femur and why?
The femur contains red marrow. This is as the body increases erythropoiesis to alleviate tissue hypoxia.
