| ironjustice@aol.com 2006-08-09, 8:25 am |
| <<snip>>
the administration of antioxidants is a viable untried alternative for
preventing or ameliorating autoimmune disease
<<snip>>
Oxidatively modified autoantigens in autoimmune diseases.
Kurien BT, Hensley K, Bachmann M, Scofield RH
Free Radic Biol Med. 2006 Aug 15; 41(4): 549-56
Free radical-mediated oxidative damage and consequent protein
modification by the end products of oxidative damage are important
mediators of cell toxicity and disease pathogenesis. Aldehydic
products, mainly the 4-hydroxy-2-alkenals, form adducts with proteins
and make them highly immunogenic. Oxidative modification of proteins
has been shown to elicit antibodies in a variety of diseases including
systemic lupus erythematosus (SLE), alcoholic liver disease, diabetes
mellitus (DM), and rheumatoid arthritis (RA). Oxidatively modified DNA
(8-oxodeoxyguanine) and low-density lipoproteins (LDL) occur in SLE, a
disease in which premature atherosclerosis is a serious problem. In
addition, immunization with 4-hydroxy-2-nonenal (HNE)-modified 60-kDa
Ro autoantigen elicits an accelerated epitope spreading in an animal
model of SLE. Advanced glycation end product (AGE) pentosidine and
AGE-modified IgG have been shown to correlate with RA disease activity.
Oxidatively modified glutamic acid decarboxylase is important in type 1
DM, while autoantibodies against oxidized LDL are prevalent in Behcet's
disease. The fragmentation of scleroderma-specific autoantigens occurs
as a result of oxidative modification and is thought to be responsible
for the production of autoantibodies through the release of cryptic
epitopes. In the face of overwhelming evidence for the involvement of
oxidative damage in autoimmunity the administration of antioxidants is
a viable untried alternative for preventing or ameliorating autoimmune
disease, although results in cardiovascular disease are disappointing.
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Tom
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