Influence of in vitro low-level gamma-radiation on the UV-induced DNA repair capacity of human lymphocytes - analysed by unscheduled DNA synthesis (UDS) and comet assay

1998 ◽  
Vol 37 (4) ◽  
pp. 267-275 ◽  
Author(s):  
M. N. Mohankumar ◽  
Solomon F. D. Paul ◽  
P. Venkatachalam ◽  
R. K. Jeevanram
Keyword(s):  
Dna Repair ◽  
Comet Assay ◽  
Gamma Radiation ◽  
Dna Synthesis ◽  
Human Lymphocytes ◽  
Unscheduled Dna Synthesis ◽  
Repair Capacity ◽  
Low Level ◽  
Dna Repair Capacity

Down-regulation of DNA repair in human CD34+progenitor cells corresponds to increased drug sensitivity and apoptotic response

Blood ◽  
2002 ◽  
Vol 100 (3) ◽  
pp. 845-853 ◽  
Author(s):  
Claudia Buschfort-Papewalis ◽  
Thomas Moritz ◽  
Bernd Liedert ◽  
Jürgen Thomale
Keyword(s):  
Dna Repair ◽  
Comet Assay ◽  
Alkylating Agents ◽  
Reaction Products ◽  
Repair Capacity ◽  
Dna Repair Capacity ◽  
Repair Processes ◽  
Human Cd34 ◽  
Cd34 Cells ◽  
Cell Fractions

Abstract Although DNA repair processes have been shown to considerably modulate the cytotoxic effects of alkylating agents, little information is available on the role of these mechanisms in chemotherapy-induced myelosuppression. Therefore, we have analyzed in detail the DNA repair capacity of primary human hematopoietic cells from cord blood (CB) or bone marrow (BM) by 2 functional assays, the immunocytologic assay (ICA) and single-cell gel electrophoresis (comet assay). Besides substantial interindividual differences, we consistently observed significantly lower repair capacity of CD34+ cells in comparison to CD34−, CD19+, or CD33+ cells of the same donor. After exposure to the alkylating agent ethylnitrosourea (EtNU), the comet assay displayed on average twice as many DNA single-strand breaks (SSBs) in CD34+ cells and a tripled half-life of these lesions in comparison to corresponding CD34− cells. Similarly, reduced SSB repair activity in CD34+ cells was detected following melphalan or cisplatin application. When specific antibodies were used to monitor DNA reaction products of these drugs, adduct levels were significantly higher and lesions persisted longer in the CD34+ fraction. To assess the contribution of individual pathways to overall DNA repair, modulators blocking defined steps in repair processes were coapplied with alkylating drugs. Similar “modulation pattern” in corresponding CD34+ and CD34− cell fractions indicated a generalized reduction in DNA repair capacity of CD34+ cells, rather than deficiencies in a specific pathway. Because CD34+ cells also displayed higher frequencies of apoptosis in response to melphalan or cisplatin, these findings may help to explain the myelosuppression after exposure to alkylating agents.

Unprogrammierte DNA-Synthese (DNA-Reparatur) in Milz-und Thymuszellen der Ratte nach Einwirkung von UV-Licht, Röntgenstrahlen oder Methylmethansulfonat in vitro / Unscheduled DNA Synthesis (DNA-Repair) within Splenic and Thymic Cells of the Rat under the Influence of UV-Light, X-Irradiation and/or Methyl-methanesulfonate

1980 ◽  
Vol 35 (1-2) ◽  
pp. 106-111 ◽  
Author(s):  
K. Tempel
Keyword(s):  
Dna Repair ◽  
Dna Synthesis ◽  
Excision Repair ◽  
Uv Light ◽  
Methyl Methanesulfonate ◽  
X Rays ◽  
Unscheduled Dna Synthesis ◽  
Splenic Cells ◽  
X Irradiation

Abstract DNA -Repair, Splenocytes, Thymocytes, Irradiation, Methyl-M ethanesulfonate Unscheduled DNA synthesis (UDS) of splenic and thymic cells of the rat has been stimulated in vitro by UV-light (8-128 J × m-2), X-rays (120-3480 rd), methyl-methanesulfonate (MMS), and/or a combination of UV-light and X -irradiation. The height of U DS-induced stim ulation of incorporation of [3H] thymidine into splenic and thymic cell DNA at saturation doses of UV-light (splenic cells: 8, thymic cells: 96 J × m-2) or X -irradiation (splenic cells: 960, thymic cells:~3480 rd) suggest that the greater sensitivity of T-cells (represented by thymic cells) towards UV-light and the greater sensitivity of B-cells (represented by splenic cells) towards X-rays can be explained - at least partly - in terms of less efficient excision repair systems.

Occupational and in vitro exposure to styrene assessed by unscheduled DNA synthesis in resting human lymphocytes

1982 ◽  
Vol 3 (6) ◽  
pp. 681-685 ◽  
Author(s):  
Ronald W. Pero ◽  
Tomas Bryngelsson ◽  
Benkt Högstedt ◽  
Bengt Åkesson
Keyword(s):  
Dna Synthesis ◽  
Human Lymphocytes ◽  
Unscheduled Dna Synthesis ◽  
In Vitro Exposure

A Review of the Genotoxicity of Triallate

2003 ◽  
Vol 22 (3) ◽  
pp. 233-251 ◽  
Author(s):  
Charles E. Healy ◽  
Larry D. Kier ◽  
Fabrice Broeckaert ◽  
Mark A. Martens
Keyword(s):  
Dna Synthesis ◽  
Mammalian Cells ◽  
Mutagenic Activity ◽  
Human Lymphocytes ◽  
In Vivo Studies ◽  
Weight Of Evidence ◽  
Unscheduled Dna Synthesis ◽  
Vitro Assay

Triallate is a selective herbicidal chemical used for control of wild oats in wheat. It has an extensive genotoxicity database that includes a variety of in vitro and in vivo studies. The chemical has produced mixed results in in vitro assay systems. It was genotoxic in bacterial mutation Ames assays, predominantly in Salmonella typhimurium strains TA100 and TA1535 in the presence of S9. Weaker responses have been observed in TA100 and TA1535 in the absence of S9. Mixed results have been observed in strain TA98, whereas no genotoxicity has been observed in strains TA1537 and TA1538. The presence and absence of S9 and its source seem to play a role in the bacterial response to the chemical. There have also been conflicting results in other test systems using other bacterial genera, yeast, and mammalian cells. Chromosome effects assays (sister-chromatid exchange and cytogenetics assays) have produced mixed results with S9 but no genotoxicity without S9. Triallate has not produced any genotoxicity in in vitro DNA damage or unscheduled DNA synthesis assays using EUE cells, human lymphocytes, and rat and mouse hepatocytes. In a series of in vivo genotoxicity assays (cytogenetics, micronucleus, dominant lethal, and unscheduled DNA synthesis), there has been no indication of any adverse genotoxic effect. Metabolism data indicate that the probable explanation for the differences observed between the in vitro studies with S9 and without S9 and between the in vitro and the in vivo studies is the production of a mutagenic intermediate in vitro at high doses of triallate is expected to be at most only transiently present in in vivo studies. The weight of evidence strongly suggests that triallate is not likely to exert mutagenic activity in vivo due to toxicokinetics and metabolic processes leading to detoxification.

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