Free radical mediated peroxidative damage in systemic lupus erythematosus

Life Sci. 2003 Aug 15;73(13):1655-66. doi: 10.1016/s0024-3205(03)00475-2.


Free radicals and damage caused by these molecular species are implicated in the pathogenesis of a variety of diseases, including autoimmune. Here we have examined oxidative damage, SOD activity and autoantibodies against SOD in systemic lupus erythematosus (SLE), a multifactorial disease with autoantibody production as an universal feature. We found significantly increased amounts of conjugated dienes in the SLE patients compared to normals (mean value of 0.917 vs 0.627, p = 0.0001) and MDA formation (6.96 vs 4.17 nmoles/microl, p = 0.0006) as well as decreased SOD activity. In addition, we found autoantibodies binding SOD by both ELISA and immunoblot. The presence of anti-SOD antibodies was associated with increased free radical damage in SLE patients. Heat inactivated anti-SOD autoantibodies were able to inhibit the activity of the enzyme. We propose that the inhibition of SOD by autoantibodies is, in part, responsible for the increased free radical damage seen in the disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Autoantibodies / immunology
  • Enzyme-Linked Immunosorbent Assay
  • Free Radicals / immunology
  • Free Radicals / metabolism*
  • Humans
  • Lipid Peroxidation* / immunology
  • Lipid Peroxides / blood
  • Lupus Erythematosus, Systemic / blood
  • Lupus Erythematosus, Systemic / immunology
  • Lupus Erythematosus, Systemic / metabolism*
  • Malondialdehyde / metabolism
  • Superoxide Dismutase / immunology
  • Superoxide Dismutase / metabolism
  • Thiobarbituric Acid Reactive Substances / analysis


  • Autoantibodies
  • Free Radicals
  • Lipid Peroxides
  • Thiobarbituric Acid Reactive Substances
  • Malondialdehyde
  • Superoxide Dismutase