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Superoxide dependent iron release from ferritin in inflammatory diseases
P Biemond1, A J Swaak, H G van Eijk
1Department of Biochemistry I, Medical Faculty, Erasmus University, Rotterdam, The Netherlands.
Free Radical Biology & Medicine
|January 1, 1988
Summary
Oxygen free radicals contribute to rheumatoid arthritis (RA) pathogenesis by damaging tissue. While protective factors exist, they are insufficient, and iron exacerbates radical toxicity, suggesting new treatment targets.
Area of Science:
- Rheumatology
- Immunology
- Biochemistry
Background:
- Rheumatoid arthritis (RA) pathogenesis involves complex inflammatory processes.
- Oxygen free radicals, particularly superoxide, are implicated in RA.
- Tissue damage characteristic of free radical activity is observed in RA patients.
Purpose of the Study:
- To investigate the role of oxygen free radicals in rheumatoid arthritis (RA) pathogenesis.
- To explore the interaction between iron and free radicals in RA.
- To evaluate the potential of iron chelators as a therapeutic strategy for RA.
Main Methods:
- Analysis of polymorphonuclear leucocytes (PMN) and macrophages in synovial fluid and membrane.
- Assessment of tissue damage related to free radical attack.
- Investigation of iron's role in exacerbating superoxide toxicity and hydroxyl radical formation from ferritin.
Main Results:
- Superoxide production by PMN and macrophages confirmed in RA.
- Available protective factors are insufficient to neutralize all formed radicals.
- Iron increases superoxide toxicity and can be released from ferritin, facilitating hydroxyl radical formation.
Conclusions:
- Oxygen free radicals and iron play a significant role in RA pathogenesis.
- Iron chelators represent a potential therapeutic avenue for RA, despite initial challenges with desferrioxamine.
- The free radical-ferritin interaction may be relevant in other inflammatory conditions like lupus erythematosus and hepatitis.