• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Lipid peroxidation
 

Lipid peroxidation

on

  • 150 views

 

Statistics

Views

Total Views
150
Views on SlideShare
150
Embed Views
0

Actions

Likes
0
Downloads
0
Comments
0

0 Embeds 0

No embeds

Accessibility

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Lipid peroxidation Lipid peroxidation Presentation Transcript

    • • The oxygen is needed for each living organism for survival .but oxygen is toxic as well. According to Salvemini oxygen is double edge sword :it is vital for life but leads to formation of toxic by products such as superoxide (o- 2) anion. oxygen more prone to produce superoxide radicals because molecular oxygen contain two unpaired electrons with parallel spins Free radicals
    • • These unpaired electrons reside in separate orbitals unless their spins are opposed. Reduction of o2 by direct insertion of a pair of electrons,e- ,into its partially filled orbitals is not possible without inversion of one electronic spin and such inversion of spin is a slow process
    • hence electrons are added molecular oxygen as single electron molecule when oxygen molecule takes up one electron,by univalent reduction,it becomes ”superoxide” anion O-2. O2 + e- O2 ‑
    • Ionizing radiation (x-rays and UV) can lyse water, leading to the formation of hydroxyl radicals. Transition metal ions, including Cu+ , Co2+ , Ni2+ and Fe2+ can react nonenzymically with oxygen or hydrogen peroxide, again leading to the formation of hydroxyl radicals. There Are Multiple Sources of Oxygen radicals in the Body
    • Peroxidation (auto-oxidation) of lipid exposed to oxygen is responsible not only for deterioration of foods (rancidity), but also for damage to tissues in vivo, where it may be a cause of cancer, inflammatory diseases, atherosclerosis, and aging. The deleterious effects ae considered to be caused by free radicals (ROO* , RO* , OH* ) produced LIPID PEROXIDATION IS A SOURCE OF FREE RADICALS
    • During peroxide formation from fatty acid containing methylene-interrupted double bonds, that is, those found in the naturally occurring polyunsaturated fatty acids. Lipid peroxidation is a chain reaction providing a continuous supply of free radicals that initiate future peroxidation and thus has potentially devastating effects. The whole process can be depicted as follows:
    • 1. Initiation: ROOH + Metal(n)+ → ROO* + Metal(n-1)+ + H+ X* + RH→ R* + XH 2. Propagation: R* + O2 → ROO* ROO* + RH → ROOH + R*, etc 3. Termination: ROO* + ROO* → ROOR + O2 ROO* + R* → ROOR R* + R* → RR
    • Free radicals are highly reactive molecular species with an unpaired electron; they persist for only a very short time (of the order of 10-9 to 10-12 sec) before they collide with another molecule and either abstract or donate an electron in order to achieve stability. Free Radical Reactions Are Self- Perpetuating Chain Reactions
    • Free radicals are formed in the body under normal conditions. They cause damage to nucleic acids, proteins, and lipids in cell membranes and plasma lipoproteins. This can cause cancer, atherosclerosis and coronary artery disease, and autoimmune diseases. BIOMEDICAL IMPORTANCE
    • • Interaction between antioxidants in the lipid phase (cell membranes) and the aqueous phase (cytosol). • (R•, free radical; PUFA-OO•, peroxyl radical of polyunsaturated fatty acid in membrane phospholipid; PUFA-OOH, hydroxyperoxy polyunsaturated fatty acid in membrane phospholipid, released into the cytosol as hydroxyperoxy polyunsaturated fatty acid by the action of phospholipase A2; PUFA-OH, hydroxy polyunsaturated fatty acid; Toc-OH vitamin E [ -tocopherol]; TocO•, tocopheroxyl radical; Se, selenium; GSH,
    • • reduced glutathione; GS-SG, oxidized glutathione, which is reduced to GSH after reaction with NADPH, catalyzed by glutathione reductase; PUFA-H, polyunsaturated fatty acid.)
    • • Antioxidant and Pro-Oxidant Roles of Vitamin C • Antioxidant roles: • Ascorbate + O2 – H2O2 + monodehydroascorbate; catalaseand peroxidases catalyze the reaction: 2H2O2 2H2O + O2Ascorbate + OH H2O + monodehydroascorbate
    • • Pro-oxidant roles: – Ascorbate + O2 O2– + monodehydroascorbate Ascorbate + Cu2+ Cu++ monodehydroasacorbate Cu+ + H2O2 Cu2+ + OH– + OH
    • In so doing, they generate a new radical from the molecule with which they collided. The most damaging radicals in biological systems are oxygen radicals especially superoxide, O2 -, hydroxyl, OH., and perhydroxyl, O2H., Tissue damage caused by oxygen radicals in often called oxidative damage, and factors that protect against oxygen radical damage are known as antioxidants.
    • • superoxide dismutase:this enzyme is present In both cytosol and mitochondria.It can destroy superoxide anionsO- 2 • 2H+ +2O- 2 superoxidedismutase H2O2+O2 Scavengers of free radicals
    • • The enzyme is present in all major aerobic tissues protecting aerobic organisms against the potential toxic effects of superoxide anion O- 2 .
    • • Catalase • This enzyme having high Km value situated close to aerobic dehydrogenases , like liver peroxisomes, can destroy H2o2 formed in the tissues to O2. • H2o2+H2O2 CATALASE 2H2O+O2
    • • Glutathuone Peroxidase: • When H2O2 level is less than optimum requird forhydrogenperoxidatio by catalase,the selenium containing enzyme Glutathione peroxidase can destroyH2O2with reduced gluthion(G-SH),having low Km,present in cytosole and mitochondria • H2O2+2G-SH G-S-S-G + 2H2O • Reduced glutathione oxidized glutathione