349-356Lipid peroxidation is an
important process in oxygen toxicity. Free radicals inflict this damage by
attacking polyunsaturated fatty acids, thus setting off a deleterious chain
reaction that ultimately results in their disintegration into malondialdehye, 4
hydroxy-2-nonenal and other harmful by-products. Peroxidation of lipids has
been implicated in several diseases including systemic lupus erythematosus
(SLE). SLE is an autoimmune disorder with unknown aetiology, characterized by
the presence of autoantibodies to self-antigens. There is a significant
increase in the production of free radicals like superoxide and hydroxyl
radicals in SLE. Indices of lipid peroxidation, like conjugated dienes,
malondialdehyde, 8-isoprostaglandin F2 alpha are significantly elevated in SLE.
Increased ceruloplasmin levels and decreased transferrin levels in the sera of
SLE patients have also been described. The activities of the antioxidant
enzymes superoxide dismutase, catalase and glutathione peroxidase and the
amounts of the antioxidant reduced glutathione are also significantly altered
in this disease. In addition, there are significant changes in the essential
fatty acid profile in the sera of those affected with the disease. In animal
models of the disease, immunization of mice with peptides derived from
autoantigens induces SLE like disease. Immunization with an oxidatively
modified autoantigen led to the rapid development of autoimmunity compared to
immunization with the unmodified autoantigen. Thus, oxidative damage appears to
play an important role in SLE pathogenesis