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DNA double-strand breaks induced in normal human cells during the repair of ultraviolet light damage.
Author(s) -
Matthews O. Bradley,
Victoria I. Taylor
Publication year - 1981
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.78.6.3619
Subject(s) - xeroderma pigmentosum , ultraviolet light , pyrimidine dimer , dna repair , microbiology and biotechnology , dna , biology , dna damage , nucleotide excision repair , chemistry , genetics , photochemistry
DNA double-strand breaks (DSBs) are formed in normal human IMR-90 cells during repair incubation after 100 and 300 J.m-2 of ultraviolet light. By contrast, no DSBs are formed after exposure to ultraviolet light in human XPA cells (from a patient with xeroderma pigmentosum complementation group A), which are unable to excise pyrimidine dimers. The DSBs are not due to immediate cell death, because all the cells excluded trypan blue at the time of assay and because XPA cells, which are much more sensitive to ultraviolet light than are IMR-90 cells, did not form DSBs after exposure to ultraviolet light. The DSBs do not appear to be due to either DNA synthesis or cellular single-strand endonucleases. We suggest that repair-induced DSBs would be potent lesions that might lead to cytotoxicity, chromosome aberrations, deletion mutations, and perhaps cellular transformation.

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