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  • Mitochondrial Damage Dysfunction

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    Abu Hurara
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    1. Mitochondrial damage and dysfunction can lead to the production of reactive oxygen species (ROS) through abnormal oxidative phosphorylation. 2. ROS cause cell injury through lipid peroxidation of membranes and cross-linkage alterations that can directly or indirectly damage proteins and DNA. 3. Phagocytic leukocytes like neutrophils and macrophages also produce ROS through respiratory bursts that act as weapons in host defense but can also contribute to cell injury.

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    1. Mitochondrial damage and dysfunction can lead to the production of reactive oxygen species (ROS) through abnormal oxidative phosphorylation. 2. ROS cause cell injury through lipid peroxidation of membranes and cross-linkage alterations that can directly or indirectly damage proteins and DNA. 3. Phagocytic leukocytes like neutrophils and macrophages also produce ROS through respiratory bursts that act as weapons in host defense but can also contribute to cell injury.

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    16 views4 pages

    Mitochondrial Damage Dysfunction

    Uploaded by

    Abu Hurara
    1. Mitochondrial damage and dysfunction can lead to the production of reactive oxygen species (ROS) through abnormal oxidative phosphorylation. 2. ROS cause cell injury through lipid peroxidation of membranes and cross-linkage alterations that can directly or indirectly damage proteins and DNA. 3. Phagocytic leukocytes like neutrophils and macrophages also produce ROS through respiratory bursts that act as weapons in host defense but can also contribute to cell injury.

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    © All Rights Reserved
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    of 4

    Mitochondrial DAMAGE,dysfunction

    • Abnormal oxidative phosphorylation Lead to ROS


    • Often associated with formation high conductance channel

    Transition process

    1. Opening of these channel lead to the loss of MP (Mitochondrial permeability)


    2. PH change

    ➢ Protein release etc

    Infux of Calcium
    Hypoxia Ischemia

    Depleting extracellularc calcium

    Extracellular calcium level

    Release of calcium from


    intracellular

    Cyloslolic (Ca)2+

    Induce
    apoptosis
    Number of enzyme
    activation
    Carpases increase mitochondrial permeability
    Accumulation of Oxygen derived free radical

    ➢ Oxidation Reduction reaction → O → produce H 2O → This reaction is


    imperfect

    -→ Short lived → Toxic intermediate are produced → Superoxide → H 2 O 2 → in

    Presence of fe 2+ → °OH → In felton reaction

    ➢ ROS produced → In pagocylic leucocytes → Neutrophils

    Macrophages
    Information  Destroying ingesting molecules  Weapons
    Host defense

    Phagosome similar to mitochondria → Respiratory burst membrane → cause generation

    →Superoxide O 2 → H 2 O → Hypo chlorite ( highly reactive compound )

    Enzyme Myloperoxidaze

    ➢ NO Nitric oxide → Produced in leucocytes → React O 2 → Peroxynitrole

    → Highly reactive compound → Participate in cell injury

    ➢ Free radical production increase


    • Absorption of radiant energy ( UV,light, X- rays)
    • H 2 O ionization H* + OH
    • Carbon tetrachloride
    • Information → free radicals produced by leckocytes

    Decrease
    • Superoxide → Presence of superoxide Dismulase ( SODS)
    Increase

    • Glutathione damage ( GSH ) → Protect cell from oxidation


    • 2GSH + H 2 O 2 → GS + SG +2H 2O

    Oxidizing glutathione

    • Antioxidant → Vitamin E, A and C ,B carotene

    • 2H 2 O → 2 H 2 O → O 2 + 2H 2 O

    ROS Cause Cell injury


    Liquid peroxidation of Membrane
    • Double polyunsaturated lipid → Vulnerable → To attack → Oxygen derived free
    radicals → Lipid radical interaction → Yeild peroxidase →( themselves reactive) →
    Liytic chain reaction

    Cross linkage alter changing


    • Free radical → Promote sulfahydrate mediated → enhance or decrease→ Enzymatic

    Activity → Cross linkage alternation

    Indirectly Cause polypeptide fragmentation

    DNA Damage
    In nuclear
    • Free Radical → React with thyamine → Their DNA produce single
    In mitochondrial
    Strand break → Cause cell death

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