Biology: The Unity and Diversity of Life (MindTap Course List)
14th Edition
ISBN: 9781305073951
Author: Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr
Publisher: Cengage Learning
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Chapter 7, Problem 3DAA
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 mitochondria—and 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?
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Chapter 7 Solutions
Biology: The Unity and Diversity of Life (MindTap Course List)
Ch. 7 - Is the following statement true or false? Unlike...Ch. 7 - Glycolysis starts and ends in the ___. a. nucleus...Ch. 7 - Which of the following metabolic pathways...Ch. 7 - Which molecule does not form during glycolysis? a....Ch. 7 - Prob. 5SQCh. 7 - Which of the following reaction pathways is not...Ch. 7 - Prob. 7SQCh. 7 - Prob. 8SQCh. 7 - Prob. 9SQCh. 7 - Mitochondrial Abnormalities in Tetralogy of Fallot...
Ch. 7 - Mitochondrial Abnormalities in Tetralogy of Fallot...Ch. 7 - Mitochondrial Abnormalities in Tetralogy of Fallot...Ch. 7 - Prob. 10SQCh. 7 - Most of the energy that aerobic respiration...Ch. 7 - Prob. 12SQCh. 7 - Prob. 13SQCh. 7 - Prob. 14SQCh. 7 - Match the term with the best description. _____...Ch. 7 - Prob. 1CTCh. 7 - As you learned, membranes impermeable to hydrogen...Ch. 7 - Prob. 3CT
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- Using a generalized terminology (i.e. neither CIII nor CIV specific), explain how complex III and IV act as electron/proton charge separation device (not a proton pump) in mitochondria bioenergetics to create electron potential through the iner mitochondria membranearrow_forwardThe 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+.)arrow_forwardMitochondrial 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 +. 2. What percentage of the TF patients had mitochondria that were abnormal in size?arrow_forward
- 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 +. 1. In this study, which abnormality was most strongly associated with TF?arrow_forwardMON TRANSPORT CHAIN Intermembrane Space 3 ACP Mitochondrial Matrix FADH FAD Copyrighs 0200n Benmin Cummings an impii s Addson identify the importance to keep the electrons (e-) running through the electron transport chain. The electrons move to and join with ADP to form ATP Electron movement causes the body to take in axygen. The electrons will flow through ATP Synthase in order to make ATP The energy of the moving electrons will power the transport of H+ to the intermembrane space. Next Previous 00arrow_forwardOxidative phosphorylation generates ATP using the reducing power of [NADH, FADH2 or malate] to move electrons down a series of carriers to ultimately produce a [phosphate gradient or protons gradient] across the inner mitochondrial membrane, which is used by ATP synthase to make ATP. ATP synthase harnesses the energy stored in both [charge and concentration gradients or electostatic and van der waals interations] to achieve high energy phosphate bond synthesis. If the ion gradient across the inner membrane is dissipated by the expression of UCP1, ATP is not synthesized and [heat is generated or electron transport is blocked]. The final electron acceptor in the electron transport chain is [oxygen or carbon dioxide] with water as a product.arrow_forward
- Biochemists working with isolated mitochondria recognize five energy "states" of mitochondria, depending on the presence or absence of essential substrates for respiration-O, ADP, oxidizable substrates, and so forth. The characteristics of each state are: state 1: mitochondria alone (in buffer containing P;) state 2: mitochondria + substrate, but respiration low due to lack of ADParrow_forwardIn the eukaryotic cells, the endomembrane system Secretory vesidles Preteins syetheslzed for export Esocytosis Golgi Nucleus Rough ER Smooth ER O provide additional area where many metabolic processes occur form membranous compartments called organelles determines structures of cells greatly increase a cell's total membrane area facilitates protein synthesis Helps cells to attach to other cellsarrow_forwardReferring to the figure below, explain why NADH yields more ATP than FADH2 does. Electron-transport and proton pump Oxidative phosphorylation Outer mitochondrial membrane H* -Intermembrane H+ H+ H+ space H* H+ H+ Cytochrome c H+ COQH, CoQ UU COQH2 CoQ JU U Inner mitochondrial membrane Ht e ATPase Complex II Complex II Complex IV Complex e ADP +P - Mitochondrial matrix NADH NAD+ FADH2 FAD АТР H+ -H+ H+ H20arrow_forward
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