Free radical mediated peroxidative damage in systemic lupus erythematosus

被引:115
作者
Kurien, BT
Scofield, RH
机构
[1] Oklahoma Med Res Fdn, Arthrit & Immunol Program, Oklahoma City, OK 73104 USA
[2] Univ Oklahoma, Hlth Sci Ctr, Dept Med, Oklahoma City, OK 73104 USA
[3] Dept Vet Affairs Med Ctr, Oklahoma City, OK 73104 USA
关键词
systemic lupus erythematosus; autoantibodies; free radicals; lipid peroxidation; superoxide dismutase; MANGANESE SUPEROXIDE-DISMUTASE; EXPERIMENTAL RAT UROLITHIASIS; LIPID-PEROXIDATION; OXIDATIVE STRESS; ANTIOXIDANT DEFENSE; AUTOIMMUNE-DISEASES; IN-VIVO; AUTOANTIBODIES; PROTEINS; LIVER;
D O I
10.1016/S0024-3205(03)00475-2
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
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/mul, 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.
引用
收藏
页码:1655 / 1666
页数:12
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