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Mitochondria

The Dynamic Organelle

  • Book
  • © 2007

Overview

Editors:
  1. Stephen W. Schaffer

    1. Department of Pharmacology, University of South Alabama, Mobile, USA

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    You can also search for this editor in PubMed   Google Scholar

  2. M-Saadeh Suleiman

    1. Bristol Royal Infirmary, Bristol, UK

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    You can also search for this editor in PubMed   Google Scholar

  • Covers the emergence of mitochondria as an important regulator of cell signaling
  • Focuses on the pathophysiology of the mitochondria

Part of the book series: Advances in Biochemistry in Health and Disease (ABHD, volume 2)

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Table of contents (15 chapters)

  1. Front Matter

    Pages I-X
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  2. Mitochondrial Metabolism

    1. Front Matter

      Pages 1-1
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    2. Regulation of Mitochondrial Respiration in Heart Muscle

      • Ilmo Hassinen
      Pages 3-25

    3. Regulation of Fatty Acid Oxidation of the Heart

      • Clifford D. L. Folmes, Gary D. Lopaschuk
      Pages 27-62

    4. Regulation of Mitochondrial Fuel Handling by the Peroxisome Proliferator-Activated Receptors

      • Mary C. Sugden, Mark J. Holness
      Pages 63-95

    5. Molecular Structure of the Mitochondrial Citrate Transport Protein

      • Ronald S. Kaplan, June A. Mayor
      Pages 97-116

    6. Regulation of Pyruvate and Amino Acid Metabolism

      • Thomas C. Vary, Wiley W. Souba, Christopher J. Lynch
      Pages 117-150

    7. Amino Acids and the Mitochondria

      • Nicola King
      Pages 151-166

  3. The Dynamic Nature of the Mitochondria

    1. Front Matter

      Pages 167-167
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    2. Mechanotransduction of Shear-stress at the Mitochondria

      • Abu-Bakr Al-Mehdi
      Pages 169-181

  4. Mitochondria as Initiators of Cell Signaling

    1. Front Matter

      Pages 183-183
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    2. Formation of Reactive Oxygen Species in Mitochondria

      • Julio F. Turrens
      Pages 185-196

    3. Mitochondrial Calcium: Role in the Normal and Ischaemic/Reperfused Myocardium

      • Elinor J. Griffiths, Christopher J. Bell, Dirki Balaska, Guy A. Rutter
      Pages 197-220

    4. Mitochondrial Ion Channels

      • Brian O’Rourke
      Pages 221-238

  5. Mitochondria as Initiators of Cell Death

    1. Front Matter

      Pages 239-239
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    2. The Mitochondrial Permeability Transition Pore – from Molecular Mechanism to Reperfusion Injury and Cardioprotection

      • Andrew P. Halestrap, Samatha J. Clarke, Igor Khalilin
      Pages 241-269

    3. The Apoptotic Mitochondrial Pathway – Modulators, Interventions and Clinical Implications

      • M-Saadeh Suleiman, Stephen W. Schaffer
      Pages 271-290

    4. The Role of Mitochondria in Necrosis Following Myocardial Ischemia-Reperfusion

      • Elizabeth Murphy, Charles Steenbergen
      Pages 291-301

  6. Mitochondria as Modulators of Cell Death

    1. Front Matter

      Pages 303-303
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    2. Mitochondria and Their Role in Ischemia/Reperfusion Injury

      • Sebastian Phillip, James M. Downey, Michael V. Cohen
      Pages 305-322
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Keywords

About this book

The term mitochondrion is derived from Latin, with mitos meaning thread and chondrion meaning granules. Indeed, under the light microscope, mitochondria often appear as rods or granules within the cytoplasm. For decades after initial visualization of mitochondria by light microscopy, mitochondrial function remained clouded. However, with the development of differential centri- gation and electron microscopy, it was discovered that a chief function of the mitochondria was the generation of ATP for the remainder of the cell. For many years, the energy generating function of the mitochondria was considered the primary, if not the sole function of the mitochondria. During that period, inves- gators attempted to obtain information on the mechanism of ATP synthesis and the regulation of electron transport. In the first chapter of the book, Dr. Hassinen summarizes those studies, providing clear pictures on the transformation of reducing equivalents into a proton gradient and the mechanism by which the F F 1 0 ATPase utilizes the proton gradient to generate ATP. He also summarizes the key regulatory steps of the citric acid cycle, which is the major source of reducing equivalents for the electron transport chain. In the heart, most of the carbon that feeds into the citric acid cycle is derived from fatty acid metabolism. Although fatty acid utilization provides most of the ATP for contraction, a proper balance must be maintained between the utilization of fatty acids and that of glucose. In the second chapter, Drs.

Editors and Affiliations

  • Department of Pharmacology, University of South Alabama, Mobile, USA

    Stephen W. Schaffer

  • Bristol Royal Infirmary, Bristol, UK

    M-Saadeh Suleiman

About the editors

Dr. Stephen W. Schaffer is a professor at the University of South Alabama. He is a member of the editorial board of Molecular and Cellular Biochemistry.

Dr. M.-Saadeh Suleiman is a professor at the University of Bristol, UK. His research includes investigating the role of metabolites and ionic species in myocardial protection, with special emphasis on amino acids, mitochondria, Ca2+ loading and reactive oxygen species.

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