Premium
ULTRAVIOLET‐INDUCED CELL DEATH IS INDEPENDENT OF DNA REPLICATION IN RAT KANGAROO CELLS
Author(s) -
Miyaji Eliane N.,
Menck Carlos F. M.
Publication year - 1995
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.1751-1097.1995.tb02344.x
Subject(s) - aphidicolin , photolyase , pyrimidine dimer , biology , dna synthesis , dna , programmed cell death , dna replication , dna repair , dna damage , microbiology and biotechnology , dna polymerase , cell , biophysics , apoptosis , genetics
Rat kangaroo ( Potorous tridactylus ) cells have an efficient repair system for photoreactivation of lethal lesions induced by 254 nm UV. However, this ability is lost with increasing time after UV, being completely ineffective after 24 h. Critical events leading to UV‐induced cell death must occur within this period of time. DNA synthesis was inhibited by the DNA polymerase inhibitor aphidicolin and the loss of the capability to photorepair lethal lesions was maintained as for replicating cells. Similar data were obtained in synchronized cells UV irradiated immediately before S phase. Under the same conditions, the ability to remove cyclobutane pyrimidine dimers by photoreactivation in these cells remained unchanged 24 h after irradiation. These data indicate that the critical events responsible for UV‐induced cell death occur in the absence of DNA replication.