related to biochemistry krebs cycle ADDITIONAL QUESTIONS 1. For Mr. CALL (the de
ID: 1025005 • Letter: R
Question
related to biochemistry krebs cycle
ADDITIONAL QUESTIONS
1. For Mr. CALL (the deceased), his NAD+ and NADH levels are very different
from healthy subjects, but why isn’t his glucose level drastically different?
2. It turns out that for Mr. CALL, just before he passed away, and the cyanide had
already taken effect, his rate of Kreb’s cycle was significantly decreased. Please
propose an explanation for this.
3. Please predict the levels of FAD and FADH2 for Mr. CALL. Explain.
4. (Bonus) Please explain clearly why the glucose oxidation rate increases
significantly in DNP-treated myotubes. State clearly which metabolic pathways
will be affected by DNP and what exactly causes this effect. Hint: think of what
metabolites these myotubes are deficient in, and how a lower levels of these
metabolites activate/inhibit certain enzymes and what alternative pathways may
be chosen to make up for this deficiency.
Explanation / Answer
4)
DNP - Dinitro-phenol is a chemical compound having six different chemical substances.DNP acts as a cell toxicant because it inhibits the oxidative phosphorylation in the cell (the pathway related to energy production in a cell).
It is a synthetic lipid soluble proton ionophore, an agent which transports protons (hydrogen cations) across biological membranes, It disturbs the proton gradient across mitochondria and chloroplast membranes,as a result the proton motive force used by cell to produce ATP the chemical energy is collapsed. Instead of producing ATP, the energy of the proton gradient is lost as heat . In presence of DNP, it is not easy to maintain a proton gradient across a membrane.
DNP also acts as an uncoupling agent, it means it has the ability to separate the flow of electrons and the pumping of H+ ions for ATP synthesis. It means the energy from electron transfer cannot be used for ATP synthesis.
In oxidative phosphorylation, the flow of electrons from NADH and FADH2 to oxygen leads to the pumping of H+ from the matrix to the inner membrane space. This gradient of H+ can produce ATP by flowing through ATP synthetase in the mitochondrial inner membrane. Dinitrophenol disrupts the H+gradient reducing ATP synthesis.
The uncoupling of electron transport from ATP synthesis allows rapid oxidation of Kreb's cycle substrates , promoting mobilazation of carbohydrates and fats . Usually the regulatory pathways are so adjusted that they maintain the concentration of these substrates at a particular level. But when energy is lost in the form of heat these biosynthetic pathways gets inhibited and as a result weight loss occurs.
Myotubes are the muscle fibres formed by the fusion of myoblasts into multinucleated fibres called myotubes.
Increased energy expenditure due to increased uncoupling activity reduces the energy stores by which there is demand for more fuel. Skeletal ,muscles are important sites for the regulation of glucose metabolism. Increased uncoupling activity due to overexpression of a gene called UCP gene, induces the uncoupling activity leading to increased glucose metabolism, also Long term treatment with DNP increases lactate levels in L6 myotubes, as the cells cannot use oxidative phosphorylation so they mainly depend on glycolytic pathway to maintain ATP. Due to these factors glucose oxidation increases in DNP treated myotubes.
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