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The response of HRR-deficient Chinese hamster ovary cell line reveals significant contribution of the indirect effect from both γ-rays and α-particles on NHEJ pathway
Stockholm University, Faculty of Science, Department of Genetics, Microbiology and Toxicology. (Centre for Radiation Protection Research)
Stockholm University, Faculty of Science, Department of Genetics, Microbiology and Toxicology.
Department of Agrobiology and Agrochemistry, University of Tuscia.
Stockholm University, Faculty of Science, Department of Genetics, Microbiology and Toxicology. (Centre for Radiation Protection Research)
(English)Manuscript (preprint) (Other academic)
Abstract [en]

In order to investigate the relative involvement of the different DNA repair pathways NHEJ, HRR and BER in repair of DNA lesions of different complexity, we have compared clonogenic survival and induction of micronuclei in a panel of repair-deficient CHO cell lines after exposure to γ-rays and α-particle radiation. The complexity of the DNA lesions formed was also modified by exposures to2 MDMSO, a potent radical scavenger, which is known to interact with the lesions produced by direct hits on DNA.

The NHEJ pathway gained the most from scavenging of the free radicals after irradiation to γ-rays or α-particles as evaluated by cell survival and the yields of MN. Results presented here also implicate that clustered base damages were induced by α-radiation and contributed to the yield of DNA double-strand breaks.

Keyword [en]
ionizing radiation, indirect effect, dimethyl sulfoxide, clusterd DNA damage
National Category
Biological Sciences
Research subject
Toxicology
Identifiers
URN: urn:nbn:se:su:diva-72551OAI: oai:DiVA.org:su-72551DiVA: diva2:501942
Available from: 2012-02-14 Created: 2012-02-14 Last updated: 2012-02-16Bibliographically approved
In thesis
1. Studies of DNA repair strategies in response to complex DNA damages
Open this publication in new window or tab >>Studies of DNA repair strategies in response to complex DNA damages
2012 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The main aim of this thesis was to study the role of the indirect actions of γ-rays and α-particles on the complexity of primary DNA damages and the repair fidelity of major DNA repair pathways: non-homologous end joining (NHEJ), homologous recombination repair (HRR) and base excision repair (BER). The complexity of radiation-induced damages increases and the proximity between damages decreases with increasing LET due to formation of ionization clusters along the particle track. The complexity of damages formed can be modified by the free radical scavenger dimethyl sulfoxide (DMSO). In addition, the effects of low doses of low dose rate γ-radiation on cellular response in terms of differentiation were investigated.

Paper I investigates the role of the indirect effect of radiation on repair fidelity of HRR, NHEJ and BER when damages of different complexity were induced by radiation or by potassium bromate. We found that potassium bromate induces complex DNA damages through processing of base modifications and that the indirect effect of radiation has a high impact on the NHEJ pathway. Results in paper II confirmed our conclusions in paper I that the indirect effect from both γ-rays and α-particles has an impact on all three repair pathways studied and NHEJ benefits the most when the indirect effect of radiation is removed.

In paper III we investigated the effects of low dose/dose rate γ-radiation on the developmental process of neural cells by using cell models for neurons and astrocytes. Our results suggest that low dose/dose rate γ-radiation attenuates differentiation and down-regulates proteins involved in the differentiation process of neural cells by an epigenetic rather than cytotoxic mechanism.

Place, publisher, year, edition, pages
Department of Genetics, Microbiology and Toxicology, Stockholm University, 2012. 41 p.
Keyword
ionizing radiation, complex DNA damage, indirect effect of radiation, dimethyl sulfoxide
National Category
Cell Biology
Research subject
Molecular Genetics
Identifiers
urn:nbn:se:su:diva-72472 (URN)978-91-7447-456-5 (ISBN)
Public defence
2012-03-23, Magnélisalen, Kemiska övningslaboratoriet, Svante Arrhenius väg 16 B, Stockholm, 10:00 (English)
Opponent
Supervisors
Note

At the time of doctoral defense, the following paper was unpublished and had a status as follows: Paper 2: Manuscript.

Available from: 2012-03-01 Created: 2012-02-13 Last updated: 2012-12-14Bibliographically approved

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