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Mitochondrial Metabolism. An Approach to Disease Management

  • Book

  • July 2021
  • Elsevier Science and Technology
  • ID: 5238304

Mitochondrial Metabolism: An Approach for Disease Management covers mitotherapy from three combined perspectives, Pharmacology, Toxicology and Biochemistry. After an introduction from world-renowned experts, the book's chapters cover the balancing role in reduction/oxidation mitochondria play, mitochondria as targets for therapeutics through its metabolism, mitochondrial contributions to the cell death process, mitochondrial response to environmental toxicants, the mitochondrial role in aging, the impact of calorie restrictive diets, new advances in the identification of altered mitochondria associated signaling pathways in carcinogenesis, and much more.

This book provides bioscientists new horizons to realize the importance of mitochondria in present-day research on therapies dealing with mitochondria associated chronic diseases, including diabetes, cancer and neurodegenerative disorders.

Please Note: This is an On Demand product, delivery may take up to 11 working days after payment has been received.

Table of Contents

1. Mitochondria as balancers of reduction/oxidation for intracellular environment 2. Mitochondria as biosynthetic centers and targeted therapeutics 3. Mitochondrial contribution to cell death 4. Mitochondrial response to environmental toxicants 5. Updates on mitochondria, calorie restriction and aging 6. Mitochondrial metabolism and carcinogenesis 7. Mitochondria and cancer therapy 8. Mitochondrial metabolism in diabetes 9. Mitochondrial abnormalities in neurological disorders 10. Mitochondrial abnormalities in psychological disorders 11. Mitotherapy, an attractive avenue for the future medicine

Authors

Jalal Pourahmad Professor, Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Iran. Jalal Pourahmad - Professor, Dept. of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences. Received his Masters and PhD degrees from the University of Toronto, Canada.
His current research interests are exploring ways of decreasing the toxicity of drugs and increasing their therapeutic specificity. These methods include the use of less toxic drug analogues, antidotes, improving the nutritional status of the patient and targeting of the drug to the tissue that requires therapy. The biochemical research techniques used include the monitoring of changes in biomolecules and cellular metabolism when drugs are administered in vivo, perfused intact organs, or incubated with intact cells or subcellular fractions. His studies on the sequence of events for drug induced cytotoxicity have shown that mitochondrial toxicity and sometimes lysosomal toxicity occurs. Mitochondrial toxicity causes both reductive stress and ATP depletion which releases iron and activates oxygen. The latter causes the lysosomal reactive oxygen species formation and lysosomal membrane rupture which leads to release of deadly proteases and phospholipases. The objective of his research is to provide a useful working hypothesis to understand various disease states as well as help design safer drugs and better methods for treating diseases. Mohsen Rezaei Associate Professor, Department of Toxicology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Mohsen Rezaei, Associate Professor, Department of Toxicology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Received his PhD from the same university.
His research interests include cellular and molecular mechanisms of cell injury and programmed cell death (Mitochondria related), subcellular organelle evaluations in programmed cell death, excitotoxicity and Neuroprotection, mitochondria associated pathogenesis and treatment of Diabetes, genotoxicity and Carcinogenicity, chemoprevention and Cancer treatment (Mitochondria related), novel derivatives of natural and nutraceuticals for dealing with chronic mitochondria related diseases.