Oxidative Damage to Mitochondrial Electron Transport Chain and Oxidative Phosphorylation in Human Diseases

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Background

Cellular respiration, a fundamental process that lies at the basis of life, comprises a series of reactions occurring in the cells of organisms deriving energy from metabolizing oxygen molecules and nutrients with the production of adenosine triphosphate (ATP). This process takes place in the Mitochondrial Inner Membrane (MIM) - whose structure has been solved at high resolution only recently - thanks to the mitochondrial electron transport chain (ETC), composed of respiratory complexes I-IV, Electron Transporters Ubiquinone (coenzyme Q10), and Cytochrome c. ATP is produced by Complex V (ATP synthase) within the oxidative phosphorylation process (OXPHOS). This is made possible by a charge and proton concentration gradient generated across the MIM by the flow of electrons through the ETC complexes. ETC complexes are assembled into super-complexes reducing the leakage of electrons, as well as the generation of Reactive Oxygen Species (ROS) and protein aggregates in the MIM.

Inherited defects in ETC complexes translate into defective electron transport, ROS overproduction, and impaired ATP production in relation to O2 consumption. Both ATP shortage and redox imbalance negatively affect the viability of several cell types. ROS can both affect gene transcription and chromatin structure via redox-sensitive gene regulatory events and directly oxidize biological macromolecules. ROS-induced peroxidation of polyunsaturated fatty acids in cell membranes produces lipid peroxidation products (LPO), such as 4-hydroxy-2-nonenal and other reactive aldehydes, in turn acting as “second messengers” of ROS and creating covalent adducts with cell proteins and nucleic acids that severely affect cells viability. ETC complexes, being at the main site of LPO, are most vulnerable to their products. A vicious circle may occur where the overproduction of ROS and LPO may both cause and result in defective ETC assembly and function. Additionally, LPO can be generated endogenously in acquired disease conditions such as inflammation associated with infection, loss of tolerance to self-antigens or excessive caloric intake, or introduced exogenously in the form of food additives, water contaminants, and microparticulate air pollutants. Thus, oxidative cell and tissue damage from these sources may contribute to a broad range of multifactorial diseases involving the nervous, cardiovascular, musculoskeletal, and other organ systems, as well as chronic inflammation, autoimmunity, and cancer. Intriguing parallelism may exist between the pathogenesis of inherited, early-onset mitochondrial diseases and acquired, adult-onset degenerative diseases of various organs.

This Research Topic aims to collect Original Research, Reviews, Mini Reviews, and Perspectives that critically highlight the role of oxidative damage to ETC and OXPHOS in the pathogenesis of inherited or acquired human diseases.
Areas of interest may include, but are not limited to:
• Oxidative damage associated with inherited defects of mitochondrial ETC.
• Oxidative damage to mitochondrial ETC in neurodegenerative, cardiovascular, and musculoskeletal diseases.
• Oxidative damage to mitochondrial ETC in gastrointestinal, respiratory, endocrine, metabolic, haematological, and kidney diseases.
• Oxidative damage to mitochondrial ETC in cancer development.
• Oxidative damage to mitochondrial ETC in sepsis.
• Environmental pollutants and toxins as causes of oxidative ETC damage.
• Antioxidant pharmacological, phytochemical agents, coenzyme supplements, and molecular targeted therapies for the remediation of mitochondrial ETC dysfunctions.

Keywords: Mitochondria, damage, disease, pathogenesis, phosphorylation

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