Lipid peroxidation refers to the oxidative degradation of lipids. It is the process in
which free radicals "steal" electrons from the lipids in cell membranes, resulting in
cell damage. This process proceeds by a free radical chain reaction mechanism. It most
often affects polyunsaturated fatty acids, because they contain multiple double bonds
in between which lie methylene bridges that possess especially reactive hydrogens. As
with any radical reaction, the reaction consists of three major steps: initiation, propagation,
and termination.
Initiation Initiation is the step in which a fatty acid
radical is produced. The most notable initiators in living cells are reactive oxygen species,
such as OH· and HO2, which combines with a hydrogen atom to make water and a fatty
acid radical. Propagation
The fatty acid radical is not a very stable molecule, so it reacts readily with molecular
oxygen, thereby creating a peroxyl-fatty acid radical. This radical is also an unstable
species that reacts with another free fatty acid, producing a different fatty acid radical
and a lipid peroxide, or a cyclic peroxide if it had reacted with itself. This cycle
continues, as the new fatty acid radical reacts in the same way.
Termination When a radical reacts with a non-radical,
it always produces another radical, which is why the process is called a "chain reaction
mechanism". The radical reaction stops when two radicals react and produce a non-radical
species. This happens only when the concentration of radical species is high enough for there
to be a high probability of collision of two radicals. Living organisms have different
molecules that speed up termination by catching free radicals and, therefore, protecting the
cell membrane. One important such antioxidant is vitamin E. Other anti-oxidants made within
the body include the enzymes superoxide dismutase, catalase, and peroxidase.
Final products of lipid peroxidation The end products of lipid peroxidation are
reactive aldehydes, such as malondialdehyde and 4-hydroxynonenal, the second one being
known also as "second messenger of free radicals" and major bioactive marker of lipid peroxidation,
due to its numerous biological activities resembling activities of reactive oxygen species.
http:informahealthcare.comfra10 Hazards
If not terminated fast enough, there will be damage to the cell membrane, which consists
mainly of lipids. Phototherapy may cause hemolysis by rupturing red blood cell cell membranes
in this way. In addition, end-products of lipid peroxidation
may be mutagenic and carcinogenic. For instance, the end-product malondialdehyde reacts with
deoxyadenosine and deoxyguanosine in DNA, forming DNA adducts to them, primarily M1G.
The toxicity of lipid hydroperoxides to animals is best illustrated by the lethal phenotype
of glutathione peroxidase 4 knockout mice. These animals do not survive past embryonic
day 8, indicating that the removal of lipid hydroperoxides is essential for mammalian
life. Tests
Certain diagnostic tests are available for the quantification of the end-products of
lipid peroxidation, to be specific, malondialdehyde. The most commonly used test is called a TBARS
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. In recent years development of immunochemical detection of HNE-histidine
adducts opened more advanced methodological possibilities for qualitative and quantitative
detection of lipid peroxidation in various human and animal tissues as well as in body
fluids, including human serum and plasma samples. References
^ om . ^ "Red Cell Membrane Lipid Peroxidation and
Hemolysis Secondary to Phototherapy" Enrique M. Ostrea Jr. 11. Departments of Pediatrics,
Wayne State University School of Medicine and Hutzel Hospital, Detroit, Michigan
^ a b c Lipid peroxidation-DNA damage by malondialdehyde. Marnett LJ. Mutation research 1999 Mar 8;424(1-2):83–95.
^ Muller, F. L., Lustgarten, M. S., Jang, Y., Richardson, A. and Van Remmen, H. "Trends
in oxidative aging theories". Free Radic. Biol. Med. 43, 477–503
^ "Correlates of markers of oxidative status in the general population". American Journal
of Epidemiology 2001 Aug 15;154(4):348–56. http:www.ncbi.nlm.nih.govarticles
External links Lipid peroxidation at the US National Library
of Medicine Medical Subject Headings [1] Free Radical Research open access issue
on lipid peroxidation