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ALKALINE ELUTION STUDIES OF HEMATOPORPHYRIN‐DERIVATIVE PHOTOSENSITIZED DNA DAMAGE AND REPAIR IN CHINESE HAMSTER OVARY CELLS
Author(s) -
Blazek E. R.,
Hariharan P. V.
Publication year - 1984
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1984.tb04546.x
Subject(s) - chinese hamster ovary cell , hematoporphyrin , dna , chemistry , dna damage , nucleotide excision repair , microbiology and biotechnology , dna repair , chinese hamster , biophysics , biochemistry , biology , photodynamic therapy , organic chemistry , receptor
We have used alkaline elution to study DNA damage produced by the photosensitizer hematoporphyrin derivative (HPD) in cultured Chinese hamster cells. Dosimetry was performed by measuring fluence and calculating photon absorption by intracellular HPD. HPD photosensitization causes DNA strand breakage. These breaks are repaired by the cell, although their fractional rate of repair is smaller than that for X‐ray induced strand breaks at equivalent levels of strand breakage. The combined DNA polymerase inhibitors cytosine arabinoside and hydroxyurea suppress the repair of HPD‐photosensitized breaks more strongly than they suppress repair of X‐ray induced breaks. Addition of novobiocin to the aforementioned inhibitors causes almost total suppression of photosensitized break repair. A nucleotide excision repair system with inhibitor susceptibility similar to that of the system which removes pyrimidine dimers thus does not act upon HPD‐photosensitized damage. The repair rate and inhibitor sensitivity findings together suggest biologically important differences in the chemical nature of X‐ray induced and HPD‐photosensitized strand breaks. In addition to strand breaks, HPD photosensitization produces covalent DNA‐protein crosslinks, some of which persist through at least 90 min incubation, but which are repaired within 180 min.