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ط      Citric acid cycle, Steps and enzymes ط      Regulatory steps of CAC ط      Energetic of CAC

Citric acid cycle (CAC). ط      Citric acid cycle, Steps and enzymes ط      Regulatory steps of CAC ط      Energetic of CAC D4 231-239  ,     L2  467-469. Citric Acid Cycle (CAC). CAC is for complete oxidation of Glu (CO 2 +H 2 O) & production of further ATP in mitoch. matrix (mitosol)

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ط      Citric acid cycle, Steps and enzymes ط      Regulatory steps of CAC ط      Energetic of CAC

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  1. Citric acid cycle (CAC) ط     Citric acid cycle, Steps and enzymes ط     Regulatory steps of CAC ط     Energetic of CAC D4 231-239  ,     L2  467-469

  2. Citric Acid Cycle (CAC) CAC is for complete oxidation of Glu (CO2+H2O) & production of further ATP in mitoch. matrix (mitosol) fig6.18,  ATP is generated: by high-energy phosphate bond (1 GTP) + by reducing equivalent (3 NADH, 1 FADH2) in the elect-trans-oxid phosph sequence(mitosol) fig6.19, OA (4C) + ACoA (2C) CS-ase (–CoA)  "citroyl-SCoA as intermediate"C-ate (6C) A-tase "cis-Aconitate as intermediate" IsoC (6C) ICDH (+NADH/CO2) "oxalosuccinate as intermediate" α-KG (5C) α-KGDH (+NADH/CO2) SCoA (5C) SCoA S-tase (+GTP) "succinate phaphate as intermediate" S-ate (4C) SDH (+FADH2) F-ate (5C) F-aseM-ate (4C) MDH (+NADH/CO2) OA (4C) *Tricarboxylic Acid (TCA) cycle = Citric Acid Cycle (CAC) = Kreb's cycle

  3. Regulation and characters of Citric acid cycle ط     Inhibitors of  CAC ط     Amphibolic Nature of the cycle ط     Anapleorotic reaction of CAC ط     Reactions of CAC:  stoichametry of CAC                                     control of CAC ط     Clinical correlation                    Pyruvate Dehydrogenase deficiency                    Fumarase deficiency D4 231-239  ,     L2  467-469

  4. ACoA (2C) fate fig6.11,  a) A (acetyl) + CoA (β-ME + PA + A, R)  ACoA               b) Acetate + CoA AK (–ATP)  ACoA fig6.17,  AA, FA, Pyr     ACoA  KB (only in liver mitosol)  Cholesterol Citrate  Carbon Source of Sterols & FA biosynthesis (cytosol)  Source of Reducing Equivalent (cytosol)  Other Metabolic Pathways Allosteric Regulation (cytosol)  TCA cycle (mitosol)

  5. CAC Regulation fig6.23,   1. OA + ACoA CS-ase(–) by acylCoA, SCoA, NADH, ATP (+) by ACoA, OACitarate * fig 6.20, Citrate ===> Carbon Source / Reducing Equivalent Source / Allosteric Regulator

  6. CAC Regulation                 2. Citrate A-tase (–) by MFC-ate (aninhibitor) (+) by Fe2+ IsoCitrate * Isocitrate continues in CAC

  7. CAC Regulation                 3. IsoCitrate ICDH(–) by ATP, NADH (+) by AMP, ADP, NAD+, Ca2+α-Ketoglutarate * α-KG ===>    ammonia (urea) / AA metabolism (Glu = α-KG)

  8. CAC Regulation fig,  ICDH aPK (–) by IsoC, OA, Pyr, 3PG, PEP ICDH b ICDH bPP-tase (+) by IsoC, OA, Pyr, 3PG, PEP ICDH a

  9. CAC Regulation                 4. α-KG α-KGDH(–) by ATP, NADH, GTP, SCoA (+) by Ca2+ SCoA * fig 6.21, SCoA ===>    PCoA / heme biosynthesis / KB utilization

  10. CAC Regulation                 5. Succinyl CoA SCoA S-taseSuccinate * Succinate continues in CAC

  11. CAC Regulation 6. Succinate SDH(–) by OA, Malonate (an inhibitor) (+) by ATP, Pi, succinateFumarate * Fumarate ===>    ammonia (urea) / Glu = α-KG

  12. CAC Regulation 7. Fumarate Fumarase Malate * Malate ===>    FA synth (Citrate) / Glu (OA)

  13. CAC Regulation 8. Malate MDH(–) by NAD+ (+) by OAOA * OA ===>    Pyr (PEP) / Asp (Pyrimidines)

  14. fig, Anaplerotic reaction (CAC): Pyr Pyr C-lase (-CO2/ATP) OAPEP C-lase (CO2/Pi)  PEP Pyr Malic Enz (NADPH)  M-ate MDH (NADH) OA

  15. Clinical Correlations Fumarase Deficiency: a)  Deficiency in in both cytosolic (bld lymphocytes) and in mitosolic. b)  High F-ate in urine & 1 more of C-ate, α-KG, S-ate, M-ate. c)  Sever neurological impairment, encephalopathy & Dystonia (soon after birth). d)  F-ase Deficiency is an autosomal recessive disorder (glu replaced by gln).

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