Complex II contains one heme b moiety that is not in the direct path of electron transfer. It may serve instead to decrease the frequency with which electrons leak out of the system to produce reactive oxidative species (ROS). Discuss the correlation between a defective heme b in Complex II and the development of certain types of cancer. What are some of the mechanisms by which the oxidative stress caused by ROS is alleviated? What are some of the damaging effects of ROS? How might these damaging effects lead to cancer?

Complex II contains one heme b moiety that is not in the direct path of electron transfer. It may serve instead to decrease the frequency with which electrons leak out of the system to produce reactive oxidative species (ROS). Discuss the correlation between a defective heme b in Complex II and the development of certain types of cancer. What are some of the mechanisms by which the oxidative stress caused by ROS is alleviated? What are some of the damaging effects of ROS? How might these damaging effects lead to cancer?

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter2: Cell Physiology

Section: Chapter Questions

Problem 3TAHL

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Complex II contains one heme b moiety that is not in the direct path of electron transfer (despite what many figures found on the internet show). It may serve instead to decrease the frequency with which electrons leak out of the system to produce reactive oxidative species (ROS). Discuss the correlation between a defective heme b in Complex II and the development of certain types of cancer. Name some of the ROS and give their structures. How are ROS generated? What are some of the mechanisms by which the oxidative stress caused by ROS is alleviated? What are some of the damaging effects of ROS? How might these damaging effects lead to cancer?
In angiogenic endothelial cells, pyruvate is converted to lactate (generating 2 ATP per glucose) rather than being completely oxidized (which would generate ~32 ATP by oxidative phosphorylation). Explain why angiogenic cells generate ATP anaerobically.
Cyanide is a rapidly acting, potentially deadly chemical that can exist in various forms. If accidentally ingested or inhaled, cyanide can cause rapid death by binding to complex IV (cytochrome oxidase) of the electron transport chain in the mitochondria. A.What is the mechanism by which cyanide stops cellular respiration? Be specific. B.Does cyanide cause an effect at the beginning or the end of the cellular respiration pathway? C.Does this make a difference on the effect that this chemical can have on our cells? Why? D.How does cyanide’s course of action affect the remainder of the cellular respiration pathway? E.If a person accidentally swallows cyanide, mention a potential treatment that is currently available. What is the mechanism of action of this treatment? Be specific. Please answer completely will give rating surely All questions answers needed
Red blood cells synthesize and degrade 2,3-biphosphogylerate (2,3-BPG) as a detour from the glycolytic pathway, as shown in the figure.2,3-BPG decreases the oxygen affinity of hemoglobin by binding in the central cavity of the deoxygenated form of hemoglobin. This encourages delivery of oxygen to tissues. A defect in one of the glycolytic enzymes may affect levels of 2,3-BPG. The plot above right shows oxygen-binding curves for normal erythrocytes and for hexokinase and pyruvate kinase-deficient erythrocytes. Identify which curve corresponds to which enzyme deficiency.
The herbicide dinoseb, which was removed from the market many years ago, killed plants by uncoupling oxidative phosphorylation. Ironically, plants have embedded in the inner membrane of their mitochondria a protein named the “uncoupling protein” that essentially can carry out the same process caused by dinoseb. The mechanism of uncoupling oxidative phosphorylation involves which of the following scenarios. A. Excess electrons oxidize lipids in the mitochondrial membranes, thus destroying the electron transport chain B. Excessive oxygen is consumed via reduction to water, thus depriving the mitochondria of the ability to carry out phosphorylation that requires oxygen C. The membrane selectivity required to maintain a proton gradient is altered so the potential for driving ATP synthesis via chemiosmosis is degraded D. Uncoupling oxidative phosphorylation kicks a cell into a fermentative pathway that cannot supply sufficient ATP
The effect of ATP on the allosteric enzyme PFK-1 is shown below. For a given concentration of fructose 6-phosphate, the PFK-1 activity increases with increasing concentrations of ATP, but a point is reached beyond which increasing the concentration of ATP inhibits the enzyme. (a) Explain how ATP can be both a substrate and an inhibitor of PFK-1. How is the enzyme regulated by ATP? (b) In what ways is glycolysis regulated by ATP levels? (c) The inhibition of PFK-1 by ATP is diminished when the ADP concentration is high, as shown in the illustration. How can this observation be explained? *A graph is included for this question*
Peroxidase is an enzyme found in many organisms, from plant to humans. The function of peroxidase is to break down hydrogen peroxide, which is a toxin produced as a byproduct when oxygen is produced during respiration. Myeloperoxidase is a protein found in neutrophils and catalyzes lipid peroxidation involved in immune defense. The overproduction of myeloperoxidase has been found to function as a mediator for tissue damage in inflammatory diseases. (8 points) a. Identify two examples of environmental factors that may impact myeloperoxidase activity. Describe how each of the environmental factors would affect the reaction rate of the enzyme. b. Predict the how researchers can use myeloperoxidase activity as oxidative stress biomarkers in patients with rheumatoid arthritis. Provide reasoning to justify your prediction.
Most individuals with genetic defects in oxidative phosphorylation are found to have relatively high concentrations of alanine in their blood. how this in biochemical terms? please help :)
Citrate synthase is a nuclear-encoded enzyme of the Citric Acid Cycle. The enzyme is functional in the mitochondrial matrix. Looking at the system required for mitochondrial targeting and import of citrate synthase, which of the following statements are correct? 1. Proper import and processing of citrate synthase is dependent upon other proteins found in the mitochondria. 2. Because of the signal peptide, the mature functional enzyme is actually longer than it would be if it was coded by the organelle genome. 3. Because the citrate synthase signal peptide doesn’t have a precise amino acid signature, mutations that slightly change the primary sequence have no effect on targeting. 4. To get citrate synthase into the mitochondrial matrix requires two signal sequences: one to get it across the outer membrane and a second to get it across the inner membrane. A. 1,2 and 3 B. 1 and 3 C. 2 and 4 D. 4 only E. All of 1,2,3 and 4 are correct
Sphingosine-1-phosphate (S1P) is important for cell survival. The synthesis of S1P from sphingosine and ATP is catalyzed by the enzyme sphingosine kinase. An understanding of the kinetics of the sphingosine kinase reaction may be important in the development of drugs to treat cancer. The velocity of the sphingosine kinase reaction was measured in the presence and absence of threo-sphingosine, a stereoisomer of sphingosine that inhibits the enzyme. The results are shown below. Construct a Lineweaver-Burk plot to answer the following questions: (a) What are the apparent KM and Vmax values in the presence and absence of the inhibitor? (b) What kind of an inhibitor is threo-sphingosine? Explain.
Corticosteroids (a type of hormone), and Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are non-narcotic pain relievers. Both medications are prescribed to reduce inflammation in the body. NSAIDs such as aspirin, acetaminophen, and ibuprofen are able to reduce pain, fever, and inflammation by blocking the action of the cyclooxygenase enzyme (COX) that catalyzes the conversion of arachidonic acid into prostaglandins. Common corticosteroids include prednisone, cortisone, and methylprednisolone. Choose one of these three corticosteroids. The corticosteroid that you choose and then explain how the drug works to reduce inflammation.
Corticosteroids (a type of hormone), and Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are non-narcotic pain relievers. Both medications are prescribed to reduce inflammation in the body. NSAIDs such as aspirin, acetaminophen, and ibuprofen are able to reduce pain, fever, and inflammation by blocking the action of the cyclooxygenase enzyme (COX) that catalyzes the conversion of arachidonic acid into prostaglandins. Common corticosteroids include prednisone, cortisone, and methylprednisolone. Choose one of these three corticosteroids. Do some internet research on the corticosteroid that you choose and then explain how the drug works to reduce inflammation.