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Ultraviolet irradiation induces multiple DNA double‐strand breaks and apoptosis in normal granulocytes and chronic myeloid leukaemia blasts
Author(s) -
Bogdanov Konstantin V.,
Chukhlovin Alexei B.,
Zaritskey Andrey Yu,
Frolova Olga I.,
Afanasiev Boris V.
Publication year - 1997
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1997.2913109.x
Subject(s) - apoptosis , agarose gel electrophoresis , myeloid , microbiology and biotechnology , dna damage , immunology , peripheral blood mononuclear cell , biology , programmed cell death , in vitro , dna , cancer research , genetics
Major leucocyte subpopulations were isolated from peripheral blood of healthy donors, and patients with chronic myeloid leukaemia (CML) and chronic lymphoid leukaemia (CLL). In vitro UV irradiation was performed at the wavelength of 257 nm (UVC band). DNA double‐stranded breaks (DNAdsbs) were detected immediately after UV‐irradiation, by means of agarose gel electrophoresis. Cell viability was estimated after 18 h in culture, as relative numbers of residual non‐apoptotic cells. Evaluation of the dose–response curves revealed that normal CLL lymphoid cells showed only moderate damage after UV‐irradiation, as assessed by DNAdsbs and cell viability criteria. However, normal granulocytes and myeloid blasts from CML patients expressed a sharp increase in DNAdsbs, even at lower doses of UV‐radiation. UV‐induced amplification of endogenous oxidative systems (e.g. NADPH‐dependent oxidase) is suggested as a probable reason for enhanced DNA breakage and apoptosis in cells of the granulocytic lineage.