Submitted by Dr. Tamer Fouad, M.D.
Free radicals are a chemical species that possess an
unpaired electron in the outer shell of the molecule.
Damaging reactions of free radicals
stress is defined as the state in which the level
of toxic reactive oxygen intermediates (ROI) overcomes the endogenous
antioxidant defences of the host (Bulger
EM, Helton WS; 1998). This state results in an excess of free radicals,
which can react with cellular lipids, proteins, and nucleic acids, leading to
local injury and eventual organ dysfunction. Lipids are probably the most
susceptible biomolecule to free radical attack.
Cell membranes are a rich resource of
PUFA, which are readily attacked by oxidising agents; a process that is called
lipid peroxidation. This is particularly damaging because it is a
self-perpetuating process (Cheeseman KH,
1993). The breakdown of lipid hydroperoxides often involves transition metal
LH + R??
L? + O2?
LOO? + L'H ?
LOOH + L'?
LO?, LOO?, aldehydes.
Proteins & nucleic acids seem to be
less susceptible than PUFAs to free radicals, in that there seems to be less
possibility in the formation of rapidly progressing chain reactions.
Random attack of radicals on proteins is unlikely unless extensive.
This happens only if radicals are allowed to accumulate (which is not
likely in normal cells), or if the damage is focussed on a particular site of
the protein. One way that the damage is focused is if the protein binds a
transition metal ion (Marx G, Chevion M;
1986 and Stadtman ER, Oliver CN; 1991).
Oxidising radicals readily attack DNA if
they are formed in its vicinity as has been clearly the case demonstrated by
radiation biologists. It is therefore a vulnerable & important target. As
with proteins there seems little possibility that the damage may spread into a
chain reaction. Again for damage to occur it must either be site specific
(leading to strand breaks) or it must elude the repair systems before
replication occurs leading to mutations (Cheesman
and Slater, 1993).
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