Wavelength Dependence of Dna Incision by a Human Ultraviolet Endonuclease

Abstract

The wavelength dependence of an ultraviolet irradiation of the DNA substrate for a human endonuclease was determined. Sites of DNA incision for all UVB and UVC wavelengths examined were at cytosines which were neither cyclobutane pyrimidine dimers nor 6-4'-(pyrimidin-2-one)pyrimidines. The optimal wavelengths for formation of these cytosine photoproducts were between 270 and 295 nm. This human endonuclease therefore has a similar ultraviolet substrate specificity to endonuclease III.

RELATIVE INDUCTION OF CYCLOBUTANE DIMERS and CYTOSINE PHOTOHYDRATES IN DNA IRRADIATED in vitro and in vivo WITH ULTRAVIOLET‐C and ULTRAVIOLET‐B LIGHT

“…Mechanisms of DNA damage induction by wavelengths <310 nm are different from those associated with higher wavelengths. However, studies on wavelength dependence of photohydrate formation using monochromatic light show little difference in the induction frequency of these photoproducts by wavelengths between 295 and 310nm and those > 310 nm (Doetsch et al, 1988;Gallagher et al, 1989). (2) The earlier work used an acid-base degradation assay to quantify thymine photohydrates in DNA; we used a well-characterized enzyme (endo 111) to measure these photoproducts.…”

“…Analysis of endo I11 cleavage patterns at the DNA sequence level has yielded variable results on the spectrum of monobasic damage induced by UV light. On the one hand, endo I11 recognizes cytosine damage exclusively in a UV-irradiated segment of the human alphoid sequence (Weiss and Duker, 1986;Gallagher et al, 1989); on the other hand, although cytosine photoproducts predominated as cleavage targets for a human redoxyendonuclease analogous to endo 111, a thymine cleavage site was a "hotspot" for photoproduct formation in a SaZI-PvuI restriction fragment from plasmid pUC18 (Doetsch et af., 1988).…”

Cytosine photoproduct-DNA glycosylase in Escherichia coli and cultured human cells

“…This study of endonucleolytic incision was performed with DNA substrates irradiated at 280 nm, since that was demonstrated to be the optimal wavelength for cytosine photoproduct site formation for both endonuclease III and the human lymphoblast enzyme (Weiss et al, 1987;Gallagher et al, 1989). The maximum wavelengths for production of substrate sites for both enzymes are between 270 and 295 nm, and identical sites of cytosine cleavages were found at various UVB and UVC wavelengths (Weiss et al, 1987;Gallagher et al, 1989). This is similar to the finding of maximal incision of UV-irradiated DNA at 280 nm by a partially purified endonuclease preparation from human HeLa cells (Doetsch et al, 1988).…”

Ultraviolet Action Spectrum and Effect of EPC-K1 on Ultraviolet Radiation-induced Injury in Cultured Normal Human Epidermal Keratinocytes

“…UVB 290-320 nm radiation exposure on mouse skin is directly involved in cyclobutane pyrimidine dimer formation, which was implicated in photocarcinogenesis 24 . The optimal wavelengths for formation of cyclobutane pyrimidine dimers are 270-295 nm 25 , thus NHEK death following exposure at 269 nm could be due to DNA damage. UV radiation-induced cell injury results from DNA damage and/or photochemicalinduced oxidative stress 25,26 .…”

“…The optimal wavelengths for formation of cyclobutane pyrimidine dimers are 270-295 nm 25 , thus NHEK death following exposure at 269 nm could be due to DNA damage. UV radiation-induced cell injury results from DNA damage and/or photochemicalinduced oxidative stress 25,26 . Various chromophores contained in human skin could act as endogenous UV sensitizers of photo-oxidative stress 7,27 , by generating ROS that damage DNA and cellular membranes, and promote carcinogenesis [4][5][6][7]28 .…”