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12.5 - TCA Cycle

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  1. Front
    Krebs cycle position in metabolism
    Back
    Occurs between initial oxidations and electron transport with ATP synthesis
  2. Front
    Stages of cellular respiration
    Back
    Fuel breakdown, conversion of carbon to acetyl-CoA, oxidation of acetyl-CoA in the Krebs cycle, and ATP generation by the electron transport chain
  3. Front
    Stage 1 of respiration
    Back
    Fuel molecules are broken down
  4. Front
    Stage 2 of respiration
    Back
    Carbon from fuels is funneled into acetyl-CoA
  5. Front
    Stage 3 of respiration
    Back
    The Krebs cycle oxidizes the acetyl group
  6. Front
    Stage 4 of respiration
    Back
    The electron transport chain uses NADH and FADH₂ to make ATP
  7. Front
    Main role of the Krebs cycle
    Back
    Generates reduced electron carriers rather than directly making a large amount of ATP
  8. Front
    Main products generated by the Krebs cycle
    Back
    NADH, FADH₂, and a small amount of GTP
  9. Front
    Reduced electron carriers from the Krebs cycle
    Back
    NADH and FADH₂ produced for oxidative phosphorylation
  10. Front
    Acetyl-CoA in complete oxidation
    Back
    Any organic compound oxidized to CO₂ and H₂O must first be transformed into acetyl-CoA
  11. Front
    Importance of acetyl-CoA
    Back
    Common intermediate linking carbohydrate, fatty acid, and amino acid metabolism
  12. Front
    Molecule that enters the Krebs cycle
    Back
    Acetyl-CoA
  13. Front
    What does not enter the Krebs cycle directly
    Back
    Glucose and fatty acids do not enter directly; they must first become acetyl-CoA
  14. Front
    Krebs cycle
    Back
    Another name for the citric acid cycle or tricarboxylic acid cycle
  15. Front
    Citric acid cycle (CAC)
    Back
    Another name for the Krebs cycle
  16. Front
    Tricarboxylic acid cycle (TCA)
    Back
    Another name for the Krebs cycle
  17. Front
    Location of the Krebs cycle
    Back
    Mitochondrial matrix
  18. Front
    Krebs cycle and oxygen
    Back
    The cycle functions only in aerobic conditions because it depends indirectly on oxygen
  19. Front
    Why the Krebs cycle is aerobic
    Back
    NADH and FADH₂ produced by the cycle must be reoxidized by the respiratory chain
  20. Front
    Effect of absent oxygen on the Krebs cycle
    Back
    ETC stops, NADH accumulates, NAD⁺ falls, and the cycle slows or stops
  21. Front
    Main function of the Krebs cycle
    Back
    Oxidation of the 2-carbon acetyl group of acetyl-CoA to 2 CO₂
  22. Front
    Energy captured per turn of the Krebs cycle
    Back
    3 NADH, 1 FADH₂, and 1 GTP
  23. Front
    ATP contribution of the Krebs cycle
    Back
    Provides about 66% of total ATP production in most cells
  24. Front
    Biosynthetic role of the Krebs cycle
    Back
    Provides substrates for biosynthetic pathways
  25. Front
    Amphibolic pathway
    Back
    A pathway that is both catabolic and anabolic-supporting
  26. Front
    Why the Krebs cycle is amphibolic
    Back
    It oxidizes acetyl-CoA and also supplies intermediates for biosynthesis
  27. Front
    Overall structure of the Krebs cycle
    Back
    An 8-step circular pathway
  28. Front
    Reason it is called a cycle
    Back
    Oxaloacetate is regenerated at the end
  29. Front
    Carbon contribution of acetyl-CoA
    Back
    Provides 2 carbons to the cycle
  30. Front
    Carbon number of oxaloacetate
    Back
    4 carbons
  31. Front
    Carbon number of citrate
    Back
    6 carbons
  32. Front
    Carbon logic of the Krebs cycle
    Back
    Acetyl-CoA (2C) combines with oxaloacetate (4C) to form citrate (6C), then returns to oxaloacetate (4C)
  33. Front
    Step 1 of the Krebs cycle
    Back
    Condensation of oxaloacetate with the acetyl group of acetyl-CoA
  34. Front
    Reaction of step 1
    Back
    Oxaloacetate + acetyl-CoA + H₂O → citrate + CoA-SH
  35. Front
    Enzyme of step 1
    Back
    Citrate synthase
  36. Front
    What happens in step 1
    Back
    A 4-carbon oxaloacetate combines with a 2-carbon acetyl group to form 6-carbon citrate
  37. Front
    Physiologic direction of step 1
    Back
    Irreversible under physiological conditions
  38. Front
    Reason step 1 is strongly favored
    Back
    Oxaloacetate is usually present at low concentration and the reaction is pulled forward
  39. Front
    Importance of step 1
    Back
    A major control and regulatory point of the cycle
  40. Front
    Irreversible steps and regulation
    Back
    Irreversible steps are commonly important regulatory steps
  41. Front
    Step 2 of the Krebs cycle
    Back
    Isomerization of citrate to isocitrate
  42. Front
    Reaction of step 2
    Back
    Citrate ⇄ isocitrate
  43. Front
    Enzyme of step 2
    Back
    Aconitase
  44. Front
    Purpose of step 2
    Back
    Rearranges citrate so oxidation can occur in the next step
  45. Front
    Isomerization
    Back
    Same atoms and molecular formula with a different arrangement
  46. Front
    Products not made in step 2
    Back
    No carbon is lost, no ATP is made, and no NADH is made
  47. Front
    Step 3 of the Krebs cycle
    Back
    Oxidation of isocitrate to α-ketoglutarate
  48. Front
    Reaction of step 3
    Back
    Isocitrate + NAD⁺ → α-ketoglutarate + CO₂ + NADH
  49. Front
    Enzyme of step 3
    Back
    Isocitrate dehydrogenase
  50. Front
    Events of step 3
    Back
    Oxidation, decarboxylation, and conversion from a 6-carbon molecule to a 5-carbon molecule
  51. Front
    Oxidation event in step 3
    Back
    NAD⁺ is reduced to NADH
  52. Front
    Decarboxylation event in step 3
    Back
    One carbon is released as CO₂
  53. Front
    Importance of step 3
    Back
    First oxidative decarboxylation of the cycle
  54. Front
    Products of step 3
    Back
    1 NADH and 1 CO₂
  55. Front
    Physiologic direction of step 3
    Back
    Irreversible
  56. Front
    Why step 3 matters for regulation
    Back
    It is a major regulatory step
  57. Front
    Step 4 of the Krebs cycle
    Back
    Oxidative decarboxylation of α-ketoglutarate
  58. Front
    Reaction of step 4
    Back
    α-ketoglutarate + CoA-SH + NAD⁺ → succinyl-CoA + CO₂ + NADH
  59. Front
    Enzyme complex of step 4
    Back
    α-Ketoglutarate dehydrogenase complex
  60. Front
    Events of step 4
    Back
    Oxidation, decarboxylation, and addition of CoA
  61. Front
    Oxidation event in step 4
    Back
    NAD⁺ is reduced to NADH
  62. Front
    Decarboxylation event in step 4
    Back
    Another carbon is released as CO₂
  63. Front
    Product formed with CoA in step 4
    Back
    Succinyl-CoA, a high-energy thioester
  64. Front
    Carbon counting in step 4
    Back
    α-Ketoglutarate has 5 carbons and succinyl-CoA has 4 carbons
  65. Front
    Importance of carbon loss in step 4
    Back
    Second carbon is lost as CO₂
  66. Front
    Mechanistic similarity of step 4
    Back
    Has the same mechanism as pyruvate dehydrogenase
  67. Front
    Shared features of α-ketoglutarate dehydrogenase and pyruvate dehydrogenase
    Back
    Both are oxidative decarboxylation reactions, use multienzyme complexes, and form high-energy CoA thioesters
  68. Front
    Products of step 4
    Back
    1 NADH, 1 CO₂, and succinyl-CoA
  69. Front
    Physiologic direction of step 4
    Back
    Irreversible
  70. Front
    Step 5 of the Krebs cycle
    Back
    Conversion of succinyl-CoA to succinate
  71. Front
    Reaction of step 5
    Back
    Succinyl-CoA + GDP + Pi → succinate + GTP + CoA-SH
  72. Front
    Enzyme of step 5
    Back
    Succinyl-CoA synthetase
  73. Front
    Other name for succinyl-CoA synthetase
    Back
    Succinate thiokinase
  74. Front
    What is special about step 5
    Back
    It is the only substrate-level phosphorylation step in the Krebs cycle
  75. Front
    Why step 5 can make GTP
    Back
    Energy released from breaking the high-energy thioester bond of succinyl-CoA is captured as GTP
  76. Front
    GTP and ATP interconversion
    Back
    GTP + ADP ⇄ GDP + ATP
  77. Front
    High-yield product of step 5
    Back
    1 GTP, energetically equivalent to 1 ATP
  78. Front
    Step 6 of the Krebs cycle
    Back
    Oxidation of succinate
  79. Front
    Reaction of step 6
    Back
    Succinate + FAD → fumarate + FADH₂
  80. Front
    Enzyme of step 6
    Back
    Succinate dehydrogenase
  81. Front
    Special feature of succinate dehydrogenase
    Back
    Only Krebs cycle enzyme that is also part of the electron transport chain
  82. Front
    ETC identity of succinate dehydrogenase
    Back
    Complex II
  83. Front
    Why FAD is used in step 6
    Back
    The oxidation is not energetic enough to reduce NAD⁺
  84. Front
    Product of step 6
    Back
    1 FADH₂
  85. Front
    Malonate
    Back
    Structural analog of succinate and competitive inhibitor of succinate dehydrogenase
  86. Front
    Why malonate inhibits succinate dehydrogenase
    Back
    It resembles succinate and competes for the active site
  87. Front
    Step 7 of the Krebs cycle
    Back
    Hydration of fumarate
  88. Front
    Reaction of step 7
    Back
    Fumarate + H₂O → malate
  89. Front
    Enzyme of step 7
    Back
    Fumarase
  90. Front
    Type of reaction in step 7
    Back
    Hydration reaction
  91. Front
    Hydration reaction
    Back
    Addition of water across a double bond
  92. Front
    ATP production in step 7
    Back
    No ATP is produced
  93. Front
    NADH production in step 7
    Back
    No NADH is produced
  94. Front
    CO₂ release in step 7
    Back
    No CO₂ is released
  95. Front
    Role of step 7
    Back
    A preparation step for the final oxidation
  96. Front
    Goal of late Krebs cycle steps
    Back
    Regeneration of oxaloacetate so the cycle can continue
  97. Front
    Step 8 of the Krebs cycle
    Back
    Oxidation of malate
  98. Front
    Reaction of step 8
    Back
    Malate + NAD⁺ → oxaloacetate + NADH
  99. Front
    Enzyme of step 8
    Back
    Malate dehydrogenase
  100. Front
    What happens in step 8
    Back
    Malate is oxidized, NAD⁺ is reduced to NADH, and oxaloacetate is regenerated
  101. Front
    Thermodynamics of step 8
    Back
    Thermodynamically unfavorable
  102. Front
    Why step 8 still proceeds
    Back
    Oxaloacetate is rapidly consumed in step 1 by citrate synthase
  103. Front
    Product removal driving reaction forward
    Back
    A reaction can proceed when its product is rapidly used up in a following step
  104. Front
    High-yield product of step 8
    Back
    1 NADH
  105. Front
    Total products of one turn of the Krebs cycle per acetyl-CoA
    Back
    2 CO₂, 3 NADH, 1 FADH₂, and 1 GTP
  106. Front
    Sources of the 3 NADH in the Krebs cycle
    Back
    Step 3, step 4, and step 8
  107. Front
    Source of FADH₂ in the Krebs cycle
    Back
    Step 6
  108. Front
    Source of GTP in the Krebs cycle
    Back
    Step 5
  109. Front
    Direct ATP made by the Krebs cycle
    Back
    Very little direct ATP is produced
  110. Front
    Where most Krebs cycle energy is stored
    Back
    In NADH and FADH₂
  111. Front
    ATP equivalents from 3 NADH
    Back
    7.5 ATP
  112. Front
    ATP equivalents from 1 FADH₂
    Back
    1.5 ATP
  113. Front
    ATP equivalents from 1 GTP
    Back
    1 ATP
  114. Front
    Total ATP yield per acetyl-CoA from the Krebs cycle
    Back
    10 ATP
  115. Front
    Total ATP yield per glucose from the Krebs cycle
    Back
    20 ATP
  116. Front
    Very high-yield Krebs cycle fact
    Back
    1 acetyl-CoA yields 10 ATP
  117. Front
    Main regulatory enzymes of the Krebs cycle
    Back
    Citrate synthase, isocitrate dehydrogenase, and α-ketoglutarate dehydrogenase
  118. Front
    Inhibitors of Krebs cycle regulatory enzymes
    Back
    ATP and NADH
  119. Front
    Meaning of ATP and NADH inhibition
    Back
    Energy status is high, so the cycle slows
  120. Front
    Activators of Krebs cycle regulatory enzymes
    Back
    ADP and Ca²⁺
  121. Front
    Meaning of ADP and Ca²⁺ activation
    Back
    Energy is needed, so the cycle speeds up
  122. Front
    Core regulation logic of the Krebs cycle
    Back
    High energy slows the cycle and low energy speeds it up
  123. Front
    Effect of high ATP on the Krebs cycle
    Back
    Inhibits the cycle
  124. Front
    Effect of high NADH on the Krebs cycle
    Back
    Inhibits the cycle
  125. Front
    Effect of high ADP on the Krebs cycle
    Back
    Activates the cycle
  126. Front
    Amphibolic nature of the Krebs cycle
    Back
    The cycle is both catabolic and anabolic-supporting
  127. Front
    Amphibolic pathway
    Back
    A pathway that functions in both breakdown and biosynthesis
  128. Front
    Catabolic role of the Krebs cycle
    Back
    Breaks down acetyl-CoA to CO₂
  129. Front
    Anabolic-supporting role of the Krebs cycle
    Back
    Provides intermediates for synthesis
  130. Front
    α-Ketoglutarate anabolic use
    Back
    Can be used to make amino acids
  131. Front
    Oxaloacetate anabolic use
    Back
    Can be used to make glucose in gluconeogenesis
  132. Front
    Citrate anabolic use
    Back
    Can be used to make fatty acids
  133. Front
    Key idea of Krebs cycle amphibolic role
    Back
    The cycle is a source of building blocks as well as energy production
  134. Front
    Problem when Krebs cycle intermediates are removed for biosynthesis
    Back
    The cycle slows down
  135. Front
    Example of depletion slowing the Krebs cycle
    Back
    Removal of oxaloacetate for glucose synthesis decreases citrate formation and slows the cycle
  136. Front
    Need created by depletion of intermediates
    Back
    Krebs cycle intermediates must be replenished
  137. Front
    Anaplerotic reactions
    Back
    Reactions that refill Krebs cycle intermediates
  138. Front
    Most important anaplerotic reaction
    Back
    Pyruvate → oxaloacetate
  139. Front
    Enzyme that replenishes oxaloacetate
    Back
    Pyruvate carboxylase

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