<<snip>>
high level of oxidative stress in erythrocytes increases the production
of autoantibodies, possibly leading to an autoimmune response
<<snip>>
<<snip>>
antioxidants would prevent certain autoimmune responses
<<snip>>

Elevated oxidative stress in erythrocytes due to an SOD1 deficiency
causes anemia and triggers autoantibody production.
Iuchi Y, Okada F, Onuma K, Onoda T, Asao H, Kobayashi M, Fujii J
Biochem J. 2006 Oct 24;

Reactive oxygen species are involved in the aging process and diseases.
Despite the important role of Cu/Zn superoxide dismutase encoded by
SOD1, SOD1 -/- mice appear to grow normally under conventional breeding
conditions. We report here on a novel finding showing a distinct
connection between oxidative stress in erythrocytes and the production
of autoantibodies against erythrocytes in SOD1 -/- mice. Evidence is
presented to show that SOD1 is primarily required for maintaining
erythrocyte life span by suppressing oxidative stress. An SOD1
deficiency led to an increased erythrocyte vulnerability by the
oxidative modification of proteins and lipids, resulting in anemia and
compensatory activation of erythropoiesis. The continuous destruction
of oxidized erythrocytes appears to induce the formation of
autoantibodies against certain erythrocyte components, e.g. carbonic
anhydrase II, and the immune complex is deposited in the glomeruli. The
administration of an antioxidant, N-acetylcysteine, suppressed
erythrocyte oxidation, ameliorated the anemia, and inhibited the
production of autoantibodies. These data imply that a high level of
oxidative stress in erythrocytes increases the production of
autoantibodies, possibly leading to an autoimmune response, and that
the intake of antioxidants would prevent certain autoimmune responses
by maintaining an appropriate redox balance in erythrocytes.

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