describe the role of mitochondria in initiating apoptosis. please describe and summarize in short two paragraphs only.
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describe the role of mitochondria in initiating apoptosis. please describe and summarize in short two paragraphs only.
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- Energy production pathway is targeted by drugs in the malignent cancerous cells to control an x cancer type. Use your speculation and tell targeting and destroying which one energy producing agent of the oxidative phosphorylation will be most effected in blocking most of the energy production and why?Fo-F1 ATPase. The energy for ATP synthesis from ADP and Pi is provided by the downhill transport of protons through the rotary FoF1 ATP synthase . The enzyme has 3 alpha-beta and 12 ‘c’ subunits. The mitochondrion maintains change in membrane potential=180 mV (negative inside), pHin = 8, pHout=7, [Pi] = 3 mM and ADP is present as well. . What [ATP]/[ADP] ratio will be established at steady-state under these conditions? What would be the [ATP]/[ADP] ratio if the enzyme had only 9 ‘c’ subunits? full revolution of the crank (gamma subunit) produces 3 ATP.This UCP1 protein allows the protons (H+) of the mitochondrial intermembrane space to enter the mitochondrial matrix without going through the ATP synthase. This bypass represents a shortcut for protons and uncouples (i.e. eliminates the interrelationship between) the following two processes: The entry of protons inside the mitochondrial matrix, following their concentration gradient. The phosphorylation of ADP into ATP by the ATP synthase. It is this uncoupling that gave the protein its name: uncoupling protein 1 (UCP1). The following figure shows the location of UCP1 when it is expressed (synthesized) in the brown adipose tissues (BAT) of hibernating mammals. Question 12 Based on the UCP1 protein structure shown earlier, and based on the figure above, what type of protein is UCP1? Question 12 options: a) A primary active transporter. b) A motor protein.…
- In the mitochondrial disease MNGIE a deficiency of thymidine phosphorylase causes dTTP to accumulate in mitochondria. Describe the mechanism by which this occurs. A secondary effect is depletion of mitochondrial dCTP pools. Describe a plausible mechanism for this effect.Which statements are true? Explain why or why not.1 In normal adult tissues, cell death usually balancescell division.2 Mammalian cells that do not have cytochrome cshould be resistant to apoptosis induced by DNA damage.Mitochondrial oxidation of fatty acids is a major source of ATP, yet fatty acids can be oxidized elsewhere. What organelle, besides the mitochondrion, can oxidize fatty acids? What is the fundamental difference between oxidation oc- curring in this organelle and mitochondrial oxidation?
- The reason why the central effector molecule cytochrome c în apoptosis was not found in the many genetic screens for "death" genes that have been carried out in C. elegans3. β-oxidation of higher fatty acids:3.1. tissue and intracellular localization of the process3.2. activation of fatty acids3.3. mechanism of fatty acids transport to mitochondria with theparticipation of carnitineThe inner membrane of the mitochondria has folds called the cristae. How would the function of the mitochondria be different if the inner membrane were not folded
- Mitochondrial Abnormalities in Tetralogy of Fallot Tetralogy of Fallot (TF) is a genetic disorder in which heart malformations result in abnormal blood circulation, so oxygen does not reach body cells as it should. With insufficient oxygen to accept electrons at the end of miotchondrial electron transfer chains, too many free radicals form. This damages the mitochondriaand the cells. In 2004, Sarah Kuruvilla studied mitochondria in the heart muscle of TF patients. Some of her results are shown in FIGURE 7.13. Patient (age) SPO2(%) Mitochondrial Abnormalities in TF Number Shape Size Broken 1(5) 55 + + 2(3) 69 + + 3(22) 72 + + 4(2) 74 + + 5(3) 76 + + + 6(2.5) 78 + + + 7(1) 79 + + 8(12) 80 + + 9(4) 80 + + 10(B) 83 + + 11(20) 85 + + 12(2.5) 89 + + FIGURE 7.13 Mitochondrial changes in tetralogy of Fallot (TF). (A) Normal heart muscle. Many mitochondria between the fibers provide muscle cells with ATP for contraction. (B) Heart muscle from a person with TF has swollen, broken mitochondria. (C) Types of mitochondrial abnormalities in TF patients. SPO2 is oxygen saturation of the blood. A normal value of SPO2 is 96%. Abnormalities are marked +. 3. Can you make any correlations between blood oxygen content and mitochondrial abnormalities in these patients?The Relative Efficiency of ATP Synthesis in Noncyclic versus Cyclic Photophosphorylation If noncyclic photosynthetic electron transport leads to the translocation of 7 H+/2e- and cyclic photosynthetic electron transport leads to the translocation of 2 H+/e-, what is the relative photosynthetic efficiency of ATP synthesis (expressed as the number of photons absorbed per ATP synthesized) for noncyclic versus cyclic photophosphorylation? (Assume that the CF1CF0-ATP synthase yields 3 ATP/14 H+.)ACTIVITY4; ETC Crossword Puzzle Direction Answer the questions or complete the statements below to fill in the puzzle Across Down 3. Complex lis also known as the 1. Heptachior has been hinked to health issue complex 4. In stage of the ETC, the heptachlor is 2. is when the body has elevated levels inhibited of calcium 6. Complex Il is linked directly to the 5. Rotenone is most commonly found in cycle 8. Complex is inhibited in this pesticide, 7. Rotenone is most abundant in the part of the plant 9. There are (number) complexes in the 10. Heptachlor is commonly spread in ETC form 13. There are (number) ATP produced 11. Complex is also known as the per glucose molecule from the electron Succinate Dehydrogenase Complex transport chain 12. Heptachlor is a man-made substance. 14.type of reaction is used to transfer electrons from electron donors to electron acceptors 15. compound receives electrons from NADH 16. (plant) is where the rotenone comes from 17. in a eukaryotic cell, most of the…