In conditions in which solely monoadducts (MA) are induced in DNA, i.e., treatment with 4,5′,8-trimethylpsoralen and 405 nm radiation, Fanconi's anemia cells (FA) appear to be more sensitive than normal human fibroblasts (1 BR/3) to cytotoxicity. The repair of such induced MA is impaired in FA compared to normal cells. When increasing the proportion of DNA interstrand cross-links (CL) over MA using a reirradiation protocol, the differential sensitivity between FA and normal human cells increases. Moreover, for a constant number of total adducts or at different ratios of CL over MA, the repair of CL is systematically hampered in FA as compared to normal cells. Incision of CL being progressively diminished by increasing amounts of MA in normal cells (D. Papadopoulo, D. Averbeck, and E. Moustacchi, Photochem. Photobiol., 47: 321–326, 1988), we show here that it is even more so for FA cells.

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This work was supported by grants from CNRS, INSERM (Contract 852017), CEA (Saclay) France, and CEE Grant BIO-151 F.

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