Differential sensitivity ofXeroderma pigmentosum cells of different repair capacities towards the chromosome breaking action of carcinogens and mutagens

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Abstract
The sensitivity of cultured fibroblasts obtained from four unrelated Xeroderma pigmentosum patients (XP‐K, XP‐C, XP‐E and XP‐H), which showed different DNA repair levels, was examined. The frequency of metaphase plates with chromosome aberrations and the frequency of breaks and exchanges per chromosome complement were estimated following exposure to the carcinogens 4‐nitroquinoline‐1‐oxide (4N QO), N‐acetoxy‐2‐acetyl‐aminofluorene (N‐acetoxy‐2‐AAF), and N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG), and to the mutagen daunomycin. The frequency of chromosome aberrations (breaks and exchanges) increased in the order (XP‐K < XP‐C < XP‐E < XP‐H) with decreasing DNA repair capacity of the XP cells examined (XP‐K > XP‐C > XP‐E > XP‐H) following 4N QO and N‐acetoxy‐2‐AAF. MNNG induced DNA repair synthesis and chromosome aberrations in the four XP cell types at levels comparable to those in fibroblasts of non‐afflicted persons. Daunomycin triggered no DNA repair synthesis but induced similar frequencies of chromosome aberrations in the XP cells and controls. Heterozygous XP cells from parents of XP‐K, XP‐E and XP‐C responded as control cells towards the three carcinogens and the mutagen used. Xeroderma pigmentosum can be considered to be an “induced” chromosome instability syndrome, in contrast to Bloom's syndrome or Fanconi's anaemia, which are “spontaneous” chromosome breakage syndromes according to German's definition.

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