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Oxyradical-mediated chromosome damage in patients with familial Mediterranean fever
I Emerit1, R Arutyunyan, T Sarkisian
1Department of Genetics, Centre de Recherches Bio-médicales des Cordeliers CNRS & University of Paris, France.
Abstract:
Increased chromosome breakage is observed in patients with familial mediterranean fever (FMF). Their plasma contains clastogenic material inducing chromosome damage in cells from healthy persons. It is proposed that increased oxyradical generation by activated polymorphonuclear cells in blood and serosal fluids of these patients leads to the formation of a clastogenic factor (CF), as it is observed in other chronic inflammatory diseases. Also similar to these diseases, the clastogenic effects are prevented by superoxide dismutase and partially by inhibitors of arachidonic acid metabolism.
Insights
Familial Mediterranean Fever (FMF) patients show increased chromosome breakage due to plasma clastogenic material. This damage, linked to oxyradical generation, can be prevented by superoxide dismutase.
Area of Science:
- Genetics
- Cell Biology
- Inflammation Research
Background:
- Familial Mediterranean Fever (FMF) is associated with increased chromosome breakage.
- Plasma from FMF patients contains clastogenic material that induces DNA damage in healthy cells.
Purpose of the Study:
- To investigate the mechanism behind chromosome breakage in FMF.
- To identify the nature of the clastogenic factor (CF) in FMF plasma.
Main Methods:
- Analysis of chromosome breakage in FMF patients.
- In vitro studies using plasma from FMF patients and healthy cells.
- Assessment of the role of oxyradicals and arachidonic acid metabolism.
Main Results:
- FMF plasma contains a clastogenic factor causing chromosome damage.
- Increased oxyradical generation by polymorphonuclear cells is implicated.
- Superoxide dismutase prevented the clastogenic effects, while arachidonic acid inhibitors partially reduced them.
Conclusions:
- A clastogenic factor, likely formed by oxyradical generation from activated polymorphonuclear cells, contributes to chromosome damage in FMF.
- The findings suggest similarities with other chronic inflammatory diseases regarding DNA damage mechanisms.