HISTORY
The first studies of this lipid
oxidation problem was those of the Swiss chemist Nicolas- Theodore de Saussure
who observed around 1800 using a simple mercury manometer that a layer of
walnut oil exposed to air was able to absorb about 150 times its own volume of
oxygen during a one year period.
Parallel with these changes, oil became viscous and had a bad smell.
Later, Berzelinus (who discovered selenium) suggested that this oxidation might
be involved in the spontaneous ignition of wool lubrified with linseed oil in
textile mills. Parmenties A.A, a pharmacist who introduced potato culture in
France, hypothesize also that oxygen in combination with fats was the agent of
rancidity (Halliwell, 1985).
Systematic
studies of lipid autoxidation may be considered to have begun around the 40s
since Halliwell, (1985) established that hydrocarbon are the primary products
of hydrocarbon oxidation. Since the early 1960,s our understanding of the
oxidation of unsaturated lipids has advanced considerably as a result of the
application of new analytical tools. Detailed studies of the products of
polyunsaturated fatty acids were initiated in the 70s by several research
groups revealing more complex mixtures than those previously propose (Benzie,
1996).
With the help of HPLC, several hydro peroxide
products could be separated after autoxidation of arachidonic acid (Choo,
2003), including products of lipoxygenase action. The first demonstration of
free radical oxidation of membrane phospholipids was green in 1980 (Benzie,
1996), leading to a new fruitful era with a continuous flow of innumerable
works devoted to chemistry, biochemistry and medicine.
MECHANISM OF LIPID PEROXIDATION
Lipid peroxidation refers to oxidative
degradation of lipids. it is the process whereby free radicals “steal”
electrons from the lipids in cell membranes, resulting in cell damage
(Benize,1996). This process proceeds by a free radical chain reaction
mechanism. Most often, it affects polyunsaturated fatty acids because they
contain multiple double bonds in between which the methylene –CH2- groups attach
especially the reactive hydrogens. As with any radical reaction, the reaction
consists of three major steps; - initiation, propagation and termination.
INITIATION
Initiation
is the step whereby a fatty acid radical is produced (Benzie, 1996). Lipid hydro peroxides are non- radical
intermediates derived from unsaturated fatty acids, phospholipids, glycolipids,
cholesterol esters and cholesterol itself. There formation occur in enzymatic
or non- enzymatic reactions involving activated chemical species known as
reactive oxygen species (ROS) which are responsible for toxic effects in the
body via various tissue damage (Halliwell, 1985). These ROS include among
others hydroxyl radicals, lipid oxyl or peroxyl radicals, singlet oxygen and
peroxinitrite form, nitrogen oxide (NO), all these groups of atoms behave as a
unit and are now named “free radical” (Choo et al, 2003).
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 too is an unstable species that react with
another fatty acid producing a different fatty acid radical and a hydrogen
peroxide or a cyclic peroxide if it had reacted with itself (Benzie, 1996) this
cycle continues as the new fatty acid radical reacts in the same way.
TERMINATION
When a radical reacts 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 (Enrique et al, 2007). This happens only when the
concentration of radical species is high enough for there to be a high
probability of two radicals actually colliding.
Living
organisms have evolved different molecules that speed up termination by catching
free radicals and therefore protect the cell membrane. One important of such
antioxidant is alpha-tocopherol, also known as vitamin E. other antioxidants
made within the body include the enzymes super oxide dismutase, catalase and
peroxidase (Enrique et al 2007). In conclusion, lipid peroxidation if not
terminated fast enough will bring damage to the cell membranes, which consists
mainly of lipids (Enrique et al, 2007). In addition, end products of lipid
peroxidation may be mutagenic and carcinogenic and phototherapy may cause
hemolysis by rupturing red blood cell and cell membranes (Enrique et al, 2007).
Certain diagnostic tests are available for the quantification of the end
product of lipid peroxidation, specifically malondialdehyde (MDA). The most
commonly used test is called a TBARS Assay.