Role of Radiation in DNA Damage and Radiation Induced Cancer

2019 ◽  
pp. 1-23
Author(s):  
Vaishali Chandel ◽  
Gaurav Seth ◽  
Priyank Shukla ◽  
Dhruv Kumar
Keyword(s):  
Dna Damage ◽  
Radiation Induced Cancer ◽  
Radiation Induced

scholarly journals Role of inhibitory CDC2 phosphorylation in radiation-induced G2 arrest in human cells.

1996 ◽  
Vol 134 (4) ◽  
pp. 963-970 ◽  
Author(s):  
P Jin ◽  
Y Gu ◽  
D O Morgan
Keyword(s):  
Dna Damage ◽  
Chromatin Condensation ◽  
S Phase ◽  
Human Cells ◽  
G2 Arrest ◽  
Hela Cell Lines ◽  
Radiation Induced ◽  
G2 Delay ◽  
In Cells

The activity of the mitosis-promoting kinase CDC2-cyclin B is normally suppressed in S phase and G2 by inhibitory phosphorylation at Thr14 and Tyr15. This work explores the possibility that these phosphorylations are responsible for the G2 arrest that occurs in human cells after DNA damage. HeLa cell lines were established in which CDC2AF, a mutant that cannot be phosphorylated at Thr14 and Tyr15, was expressed from a tetracycline-repressible promoter. Expression of CDC2AF did not induce mitotic events in cells arrested at the beginning of S phase with DNA synthesis inhibitors, but induced low levels of premature chromatin condensation in cells progressing through S phase and G2. Expression of CDC2AF greatly reduced the G2 delay that resulted when cells were X-irradiated in S phase. However, a significant G2 delay was still observed and was accompanied by high CDC2-associated kinase activity. Expression of wild-type CDC2, or the related kinase CDK2AF, had no effect on the radiation-induced delay. Thus, inhibitory phosphorylation of CDC2, as well as additional undefined mechanisms, delay mitosis after DNA damage.

The role of nucleotide excision repair of Escherichia coli in repair of spontaneous and gamma-radiation-induced DNA damage in the lacZα gene

2000 ◽  
Vol 460 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Gitta K Kuipers ◽  
Ben J Slotman ◽  
Hester A Poldervaart ◽  
Ingrid M.J van Vilsteren ◽  
Carola A Reitsma-Wijker ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Gamma Radiation ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Nucleotide Excision ◽  
Radiation Induced

830 The role of superoxide dismutase in protection against radiation-induced DNA damage

1995 ◽  
Vol 31 ◽  
pp. S174
Author(s):  
N.P. Mithal ◽  
T.J. McMillan ◽  
A. Radunovic ◽  
P.N. Leigh ◽  
G.G. Steel
Keyword(s):  
Dna Damage ◽  
Superoxide Dismutase ◽  
Radiation Induced

Modeling radiation-induced cell death: role of different levels of DNA damage clustering

2015 ◽  
Vol 54 (3) ◽  
pp. 305-316 ◽  
Author(s):  
M. P. Carante ◽  
S. Altieri ◽  
S. Bortolussi ◽  
I. Postuma ◽  
N. Protti ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Radiation Induced ◽  
Different Levels

Radiation-induced versus endogenous DNA damage: possible effect of inducible protective responses in mitigating endogenous damage

2003 ◽  
Vol 22 (6) ◽  
pp. 290-306 ◽  
Author(s):  
Myron Pollycove ◽  
Ludwig E Feinendegen
Keyword(s):  
Dna Damage ◽  
Low Dose ◽  
Published Data ◽  
Low Dose Radiation ◽  
Dna Damages ◽  
Cellular Protection ◽  
Radiation Sources ◽  
Radiation Induced Cancer ◽  
Radiation Induced ◽  
Dose Radiation

Ionizing radiation (IR) causes damage to DNA that is apparently proportional to absorbed dose. The incidence of radiation-induced cancer in humans unequivocally rises with the value of absorbed doses above about 300 mGy, in a seemingly linear fashion. Extrapolation of this linear correlation down to zero-dose constitutes the linear-no-threshold (LNT) hypothesis of radiation-induced cancer incidence. The corresponding dose-risk correlation, however, is questionable at doses lower than 300 mGy. Non-radiation induced DNA damage and, in consequence, oncogenic transformation in non-irradiated cells arises from a variety of sources, mainly from weak endogenous carcinogens such as reactive oxygen species (ROS) as well as from micronutrient deficiencies and environmental toxins. In order to relate the low probability of radiation-induced cancer to the relatively high incidence of non-radiation carcinogenesis, especially at low-dose irradiation, the quantitative and qualitative differences between the DNA damages from non-radiation and radiation sources need to be addressed and put into context of physiological mechanisms of cellular protection. This paper summarizes a co-operative approach by the authors to answer the questions on the quantitative and qualitative DNA damages from non-radiation sources, largely endogenous ROS, and following exposure to low doses of IR. The analysis relies on published data and justified assumptions and considers the physiological capacity of mammalian cells to protect themselves constantly by preventing and repairing DNA damage. Furthermore, damaged cells are susceptible to removal by apoptosis or the immune system. The results suggest that the various forms of non-radiation DNA damage in tissues far outweigh corresponding DNA damage from low-dose radiation exposure at the level of, and well above, background radiation. These data are examined within the context of low-dose radiation induction of cellular signaling that may stimulate cellular protection systems over hours to weeks against accumulation of DNA damage. The particular focus is the hypothesis that these enhanced and persisting protective responses reduce the steady state level of nonradiation DNA damage, thereby reducing deleterious outcomes such as cancer and aging. The emerging model urgently needs rigorous experimental testing, since it suggests, importantly, that the LNT hypothesis is invalid for complex adaptive systems such as mammalian organisms.

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