Aneugenic and clastogenic alterations in the DBA/IJ mouse model of rheumatoid arthritis treated with rituximab, an anti-CD20 antibody

Rheumatoid arthritis (RA), an autoimmune disorder in which the immune system attacks healthy cells, is associated with elevated risk of lymphoma. Rituximab, a treatment for non-Hodgkin's lymphoma, has been approved as a treatment for RA. We studied the effects of rituximab on chromosomal stability in collagen -induced arthritis DBA/1J animal models. Micronucleus levels were increased in the mouse models, mainly due to chromosome loss, as detected by fluorescence in situ hybridization; rituximab-treated arthritic mice had significantly less micronucleus formation. Serum 8-hydroxydeoxyguanosine, a DNA oxidative stress marker, was increased in the mice models but reduced following rituximab administration.

Automated summary

Rheumatoid arthritis (RA) is associated with increased risk of lymphoma, an autoimmune disorder. Rituximab, approved for non-Hodgkin's lymphoma, is also used to treat RA. In a study using collagen-induced arthritis DBA/1J animal models, rituximab reduced micronucleus formation caused by chromosome loss and decreased the DNA oxidative stress marker 8-hydroxydeoxyguanosine.