Several authors have suggested that the cells of patients with systemic lupus erythematosus (SLE) have defects of DNA repair. Cells from patients with the classical chromosomal instability syndromes, thought to be due to defects in DNA repair, are hypersensitive to the chromosome damaging effects of some DNA damaging agents, measured as sister chromatid exchange (SCE). We have observed that lymphocytes of patients with SLE are not more sensitive than lymphocytes from healthy individuals to the SCE inducing effects of the DNA damaging agents methyl nitrosourea, methyl methanesulphonate, chlorambucil, and bromodeoxyuridine. These observations do not support the suggestion that cells of patients with SLE have an underlying defect of DNA repair.
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