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RECOVERY FROM INHIBITION BY UV‐IRRADIATION OF ORNITHINE DECARBOXYLASE INDUCTION IN HUMAN CELLS: IMPLICATION OF EXCISION REPAIR
Author(s) -
BenHur E.,
Prager A.,
Buonaguro F.
Publication year - 1982
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.1751-1097.1982.tb02627.x
Subject(s) - ornithine decarboxylase , microbiology and biotechnology , dna synthesis , nucleotide excision repair , biology , dna , dna repair , chemistry , biochemistry , enzyme
— Exposure of stationary‐phase human breast carcinoma(T–47D) cells to far‐UV light (254 nm) inhibited the appearance of induced ornithine decarboxylase (ODC) activity. The fluence response curve had a shoulder (D 4 = 2 J m ‐2 ) followed by an exponential decline (D 0 = 4.2 Jm ‐2 ). The cells could recover from this inhibition when the stimulus of induction of ODC was delayed for20–24 h after irradiation. Hydroxyurea (HU) when present at 3 mM during the recovery period eliminated completely the ability of the cells to recover. This effect of HU on ODC induction was partially reversed by 50 nM of the four deoxyribonucleosides required for DNA synthesis. Neither HU nor the deoxyribonucleosides by themselves affected ODC induction in unirradiated cells. Since HU inhibited the recovery from potentially lethal UV damage and is a known inhibitor of excision repair, we interpret the above results to mean that recovery from UV‐induced inhibition of ODC induction depends on excision‐repair of DNA damage. This interpretation is strongly supported by the finding that specific photolysis of 5‐bromodeoxyuridine, incorporated into DNA during the recovery period, inhibited recovery of ODC induction from inhibition by UV light.