Lipid peroxidation

Source: Wikipedia, the free encyclopedia.
"LOPs" redirects here. For other uses, see LOP (disambiguation).

Lipid peroxidation, or lipid oxidation, is a complex

oxidizing agents, leading to a chain reaction that results in oxidative stress and cell damage
.

In

rancidity.[5]

Reaction mechanism

Simplified pathway for lipid autoxidation: Initiated by hydroxyl radical, which abstracts hydrogen and forms a pentadienyl radical (only one resonance structure shown). This radical adds O2 to give hydroperoxyl radical (red). In a propagation step, this hydroperoxyl radical abstracts an H+ atom from a new diene, generating a new pentadienyl radical and a hydroperoxide (blue).

The chemical reaction of lipid peroxidation consists of three phases: initiation, propagation, and termination.[4]

In the initiation phase, a

polyunsaturated fatty acid
(PUFA), to form the lipid radical (L•) and water (H2O).

In the propagation phase, the lipid radical (L•) reacts with

hydroperoxyl radical (LOO•). The lipid hydroperoxyl radical (LOO•) can further abstract hydrogen from a new PUFA substrate, forming another lipid radical (L•) and now finally a lipid hydroperoxide (LOOH).[6]

The lipid hydroperoxyl radical (LOO•) can also undergo a variety of reactions to produce new radicals.[citation needed]

The additional lipid radical (L•) continues the chain reaction, whilst the lipid hydroperoxide (LOOH) is the primary end product.[6] The formation of lipid radicals is sensitive to the kinetic isotope effect. Reinforced lipids in the membrane can suppress the chain reaction of lipid peroxidation.[7]

The termination step can vary, in both its actual chemical reaction and when it will occur.

species is high.[citation needed
]

The primary products of lipid peroxidation are lipid hydroperoxides (LOOH).[3]

Arachidonic acid as a substrate

When arachidonic acid is a substrate, isomers of hydroperoxyeicosatetraenoic acid (HPETEs) and hydroxyeicosatetraenoic acids (HETEs) are formed.[citation needed]

Role of antioxidants

Main article:
Antioxidants
Free radical mechanisms in tissue injury. Lipid peroxidation induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).

Antioxidants play a crucial role in mitigating lipid peroxidation by neutralizing free radicals, thereby halting radical chain reactions. Key antioxidants include

enzymes including superoxide dismutase, catalase, and peroxidase contribute to the oxidation response by reducing the presence of hydrogen peroxide
, which is a prevalent precursor of the hydroxyl radical (OH•).

As an example, vitamin E can donate a hydrogen atom to the lipid hydroperoxyl radical (LOO•) to form a vitamin E radical, which further reacts with another lipid hydroperoxyl radical (LOO•) forming non-radical products.[2]

Medical implications

Phototherapy may cause lipid peroxidation leading to rupture of red blood cell cell membranes in this way.[9]

In addition, end-products of lipid peroxidation may be

DNA adducts to them, primarily M1G.[10]

Reactive aldehydes can also form

Michael adducts or Schiff bases with thiol or amine groups in amino acid side chains. Thus, they are able to inactivate sensitive proteins through electrophilic stress.[11]

The toxicity of lipid hydroperoxides to animals is best illustrated by the lethal phenotype of glutathione peroxidase 4 (GPX4) knockout mice. These animals do not survive past embryonic day 8, indicating that the removal of lipid hydroperoxides is essential for mammalian life.[12]

On the other hand, it's unclear whether dietary lipid peroxides are bioavailable and play a role in disease, as a healthy human body has protective mechanisms in place against such hazards.[13]

Tests

Certain diagnostic tests are available for the quantification of the end-products of lipid peroxidation, to be specific, malondialdehyde (MDA).[10] The most commonly used test is called a TBARS Assay (thiobarbituric acid reactive substances assay). Thiobarbituric acid reacts with malondialdehyde to yield a fluorescent product. However, there are other sources of malondialdehyde, so this test is not completely specific for lipid peroxidation.[14]

See also

References

  1. ISBN 978-0-323-37468-2
    , retrieved 2024-03-15
  2. ^
    PMID 24999379
    .
  3. ^
    PMID 24278542
    .
  4. ^
    S2CID 4051766
    .
  5. ISBN 978-0-12-384953-3, archived
    from the original on 2022-05-04, retrieved 2024-03-15
  6. ^
    PMID 24999379
    .
  7. PMID 22705367
    .
  8. PMID 12197998
    .
  9. S2CID 39547619
    .
  10. ^
    PMID 10064852
    .
  11. PMID 19686040
    .
  12. PMID 17640558.{{cite journal}}: CS1 maint: multiple names: authors list (link
    )
  13. S2CID 90319530. Archived
    from the original on 2021-04-13. Retrieved 2021-04-13.
  14. PMID 11495858
    .

External links
Retrieved from "https://en.wikipedia.org/w/index.php?title=Lipid_peroxidation&oldid=1216368348"