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Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 1 лютого 2022

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1

Jalal, Nasir, Saba Haq, Namrah Anwar, Saadiya Nazeer, and Umar Saeed. "Radiation induced bystander effect and DNA damage." Journal of Cancer Research and Therapeutics 10, no. 4 (2014): 819. http://dx.doi.org/10.4103/0973-1482.144587.

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2

Kalinich, John F., George N. Catravas та Stephen L. Snyder. "The Effect of γ Radiation on DNA Methylation". Radiation Research 117, № 2 (лютий 1989): 185. http://dx.doi.org/10.2307/3577319.

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3

Rita, Ghosh, and Hansda Surajit. "Targeted and non-targeted effects of radiation in mammalian cells: An overview." Archives of Biotechnology and Biomedicine 5, no. 1 (April 12, 2021): 013–19. http://dx.doi.org/10.29328/journal.abb.1001023.

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Radiation of different wavelengths can kill living organisms, although, the mechanism of interactions differs depending on their energies. Understanding the interaction of radiation with living cells is important to assess their harmful effects and also to identify their therapeutic potential. Temporally, this interaction can be broadly divided in three stages – physical, chemical and biological. While radiation can affect all the important macromolecules of the cells, particularly important is the damage to its genetic material, the DNA. The consequences of irradiation include- DNA damage, mutation, cross-linkages with other molecules, chromosomal aberrations and DNA repair leading to altered gene expression and/or cell death. Mutations in DNA can lead to heritable changes and is important for the induction of cancer. While some of these effects are through direct interaction of radiation with the target, radiation can interact with the surrounding environment to result in its indirect actions. The effects of radiation depend not only on the total dose but also on the dose rate, LET etc. and also on the cell types. However, action of radiation on organisms is not restricted to interactions with irradiated cells, i.e. target cells alone; it also exerts non-targeted effects on neighboring unexposed cells to produce productive responses; this is known as bystander effect. The bystander effects of ionizing radiations are well documented and contribute largely to the relapse of cancer and secondary tumors after radiotherapy. Irradiation of cells with non-ionizing Ultra-Violet light also exhibits bystander responses, but such responses are very distinct from that produced by ionizing radiations.

4

Yokoya, A., N. Shikazono, K. Fujii, A. Urushibara, K. Akamatsu, and R. Watanabe. "DNA damage induced by the direct effect of radiation." Radiation Physics and Chemistry 77, no. 10-12 (October 2008): 1280–85. http://dx.doi.org/10.1016/j.radphyschem.2008.05.021.

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5

Georgakilas, Alexandros G. "Role of DNA Damage and Repair in Detrimental Effects of Ionizing Radiation." Radiation 1, no. 1 (October 22, 2020): 1–4. http://dx.doi.org/10.3390/radiation1010001.

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Ionizing radiation (IR) is considered a traditional mutagen and genotoxic agent. Exposure to IR affects in all cases biological systems and living organisms from plants to humans mostly in a pernicious way. At low (<0.1 Gy) and low-to-medium doses (0.1–1 Gy), one can find in the literature a variety of findings indicating sometimes a positive-like anti-inflammatory effect or detrimental-like toxicity. In this Special Issue and in general in the current research, we would like to acquire works and more knowledge on the role(s) of DNA damage and its repair induced by ionizing radiations as instigators of the full range of biological responses to radiation. Emphasis should be given to advances offering mechanistic insights into the ability of radiations with different qualities to severely impact cells or tissues. High-quality research or review studies on different species projected to humans are welcome. Technical advances reporting on the methodologies to accurately measure DNA or other types of biological damage must be highly considered for the near future in our research community, as well. Last but not least, clinical trials or protocols with improvements to radiation therapy and radiation protection are also included in our vision for the advancement of research regarding biological effects of IR.

6

Turaeva, N. N., S. Schroeder, and B. L. Oksengendler. "Effect of Anderson Localization on Auger Destruction of DNA." ISRN Biophysics 2012 (December 5, 2012): 1–3. http://dx.doi.org/10.5402/2012/972085.

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The effect of Anderson localization in DNA on the Auger destruction by the Coulombic explosion at ionized radiation has been theoretically discussed in the present work. The theory of Auger destruction of DNA has been modified taking into account the localized and delocalized electron states in DNA owing to the correlated disorder in a sequence of nucleotides. According to the modified theoretical model of Auger destruction, the dominant ratio of delocalized states to localized states in exon compared to intron results in stronger radiation resistance of exons to ionized irradiation causing the Auger-cascade process than the radiation resistance of introns.

7

Ganeva, Roumiana L., та Lyuben M. Tzvetkov. "Effect of Cisplatin Alone and in Combination with γ-Radiation on the Initiation of DNA Synthesis in Friend Leukemia Cells". Zeitschrift für Naturforschung C 52, № 5-6 (1 червня 1997): 405–7. http://dx.doi.org/10.1515/znc-1997-5-620.

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The effect of the anticancer drug cisplatin (alone and in combination with γ-radiation) on the initiation of DNA synthesis in Friend leukemia cells was studied. A method for isolation of DNA fractions containing the origins of replication was used. It was found that cisplatin decreased the rate of the initiation of DNA synthesis. The mild γ-radiation has previously been observed to inhibit the initiation of DNA synthesis. In the present investigation the combination of cisplatin and γ-radiation showed additive effects without synergism on the initiation of DNA biosynthesis.

8

Greubel, Christoph, Volker Hable, Guido A. Drexler, Andreas Hauptner, Steffen Dietzel, Hilmar Strickfaden, Iris Baur, et al. "Competition effect in DNA damage response." Radiation and Environmental Biophysics 47, no. 4 (July 23, 2008): 423–29. http://dx.doi.org/10.1007/s00411-008-0182-z.

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9

Bangruwa, Neeraj, Manish Srivastava, and Debabrata Mishra. "Radiation-Induced Effect on Spin-Selective Electron Transfer through Self-Assembled Monolayers of ds-DNA." Magnetochemistry 7, no. 7 (July 8, 2021): 98. http://dx.doi.org/10.3390/magnetochemistry7070098.

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Stability of the DNA molecule is essential for the proper functioning and sustainability of all living organisms. In this study, we investigate the effect of gamma radiation (γ-radiation) on spin-selective electron transfer through double strand (ds)DNA molecules. Self-assembled monolayers (SAMs) of 21-base long DNA are prepared on Au-coated Ni thin film. We measure the spin polarization (%) of the SAMs of ds-DNA using the spin-dependent electrochemical technique. We use a Cs-based γ-radiation source to expose the SAMs of ds-DNA immobilized on thin films for various time intervals ranging from 0–30 min. The susceptibility of DNA to γ-radiation is measured by spin-dependent electrochemistry. We observe that the efficiency of spin filtering by ds-DNA gradually decreases when exposure (to γ-radiation) time increases, and drops below 1% after 30 min of exposure. The change in spin polarization value is related either to the conformational perturbation in DNA or to structural damage in DNA molecules caused by ionizing radiation.

10

rezaiekahkhaie, sakine, and Khadije Rezaie Keikhaie. "The Role of Ionizing Radiation in Cellular Signaling Pathways, Mutagenesis, and Carcinogenesis." International Journal of Basic Science in Medicine 3, no. 4 (January 13, 2019): 147–53. http://dx.doi.org/10.15171/ijbsm.2018.26.

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One of the negative effects of ionizing radiation is the alteration of cellular signaling pathways which lead to carcinogenesis and tumorigenesis. In this review, we discussed the impacts of ionizing radiation on cells and cellular signaling pathways. In this regard, exposure to radiation can directly or indirectly alter cellular signaling pathways. Remarkably, irradiated cells release special mediators into cellular matrix, aberrating cell-cell and cell-environment interactions. Most notably, these mediators include nitric oxide (NO), reactive oxygen species (ROS), and cell growth factors which contribute to cellular interactions between irradiated cells and their neighbor cells, a phenomenon known as radiation-induced bystander effect. DNA molecule is the most important cellular compartment damaged by ionizing radiation. On the other hand, the ability of irradiated cells to repair the damaged DNA is very low. Therefore, DNA alternations are passed to the next generations, and ultimately lead to carcinogenesis. The study of ionizing radiations and their impacts on biological systems is of remarkable importance to divulge their impacts on cellular signaling pathways.

11

Bekturova, Assemgul, Zhannur Markhametova, and Zhaksylyk Masalimov. "Plasmids Role in Survival of Acinetobacter calcoaceticus A1 Exposed to UV-Radiation and Hydrocarbons." Advanced Materials Research 905 (April 2014): 151–55. http://dx.doi.org/10.4028/www.scientific.net/amr.905.151.

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The role of plasmids in hydrocarbon-degrading bacteriaAcinetobacter calcoaceticus A1survival to UV-radiation and hydrocarbons was studied. Natural plasmids-containingA. calcoaceticus A1showed high resistance to UV-radiation.A. calcoaceticus A1showed active growth under exposed to UV-radiation for up to 30 minutes. Combined effects of UV-radiation and petroleum hydrocarbons did not considerably reduce the growth of strains. It was shown a stimulating effect of UV-radiation on the growth curves of strains ofA. calcoaceticus A1. Constructed recombinant strain (E.coli XL blueRec) showed the ability to grow on medium with addition petroleum hydrocarbons. Combined effects of UV-radiation and petroleum hydrocarbons have had a negative effect on the growth ofE.coli XL blueRec. Thus, results showed that the plasmid DNA of natural hydrocarbon-degrading bacteriaA. calcoaceticus A1may contain genes of microbial resistance to UV - radiation and petroleum hydrocarbons.

12

Chiang, Pai-Kai, Wei-Kung Tsai, Marcelo Chen, Wun-Rong Lin, Yung-Chiong Chow, Chih-Chiao Lee, Jong-Ming Hsu, and Yu-Jen Chen. "Zerumbone Regulates DNA Repair Responding to Ionizing Radiation and Enhances Radiosensitivity of Human Prostatic Cancer Cells." Integrative Cancer Therapies 17, no. 2 (June 12, 2017): 292–98. http://dx.doi.org/10.1177/1534735417712008.

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Introduction. Radiation therapy using ionizing radiation is widely used for the treatment of prostate cancer. The intrinsic radiation sensitivity of cancer cells could be enhanced by modulating multiple factors including the capacity to repair DNA damage, especially double-strand breaks (DSBs). We aimed to examine the effect of zerumbone on radiation sensitivity and its protective effects against ionizing radiation–induced DSB in human prostate cancer cells. Materials and Methods. The human prostate cancer PC3 and DU145 cell lines were used. A colony formation assay was performed to analyze the radiation survival of cells. DNA histogram and generation of reactive oxygen species (ROS) were examined using flow cytometry. Western blotting was used to examine the expression of regulatory molecules related to DNA damage repair. Results. Pretreatment with zerumbone enhanced the radiation effect on prostate cancer cells. Zerumbone delayed the abrogation of radiation-induced expression of γ-H2AX, an indicator of DNA DSB. Zerumbone pretreatment markedly reduced ionizing radiation–induced upregulated expression of phosphorylated ATM (ataxia telangiectasia-mutated), which was partially reversed by the ATM agonist methyl methanesulfonate. Ionizing radiation augmented and zerumbone pretreatment reduced the expression of Jak2 and Stat3, which are involved in DNA damage repair signaling. No significant effect on the generation of ROS and expression of ATR was noted after zerumbone treatment. Conclusion: Zerumbone sensitized DU145 and PC3 prostatic cancer cells to ionizing radiation by modulating radiation-induced ATM activation during repair of DNA DSBs.

13

Prise, K. M., M. Folkard, H. C. Newman, and B. D. Michael. "Effect of Radiation Quality on Lesion Complexity in Cellular DNA." International Journal of Radiation Biology 66, no. 5 (January 1994): 537–42. http://dx.doi.org/10.1080/09553009414551581.

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14

Quintiliani, M. "The Oxygen Effect in Radiation Inactivation of DNA and Enzymes." International Journal of Radiation Biology and Related Studies in Physics, Chemistry and Medicine 50, no. 4 (January 1986): 573–94. http://dx.doi.org/10.1080/09553008614550981.

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15

Brabcová, Kateřina Pachnerová, Zuzana Jamborová, Anna Michaelidesová, Marie Davídková, Satoshi Kodaira, Martin Šefl, and Václav Štěpán. "RADIATION-INDUCED PLASMID DNA DAMAGE: EFFECT OF CONCENTRATION AND LENGTH." Radiation Protection Dosimetry 186, no. 2-3 (December 2019): 168–71. http://dx.doi.org/10.1093/rpd/ncz196.

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Abstract Plasmid DNA is commonly used as a simpler substitute for a cell in studies of early effects of ionizing radiation because it allows to determine yields of primary DNA lesions. Experimental studies often employ plasmids of different lengths, in different concentrations in the aqueous solution. Influence of these parameters on the heavy-ion induced yields of primary DNA damage has been studied, using plasmids pUC19 (2686 bp), pBR322 (4361 bp) and pKLAC2 (9107 bp) in 10 and 50 ng/μl concentration. Results demonstrate the impact of plasmid length, while no significant difference was observed between the two concentrations. The uncertainty of the results is discussed.

16

Pollycove, Myron, and Ludwig E. Feinendegen. "Radiation-induced versus endogenous DNA damage: possible effect of inducible protective responses in mitigating endogenous damage." Human & Experimental Toxicology 22, no. 6 (June 2003): 290–306. http://dx.doi.org/10.1191/0960327103ht365oa.

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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.

17

Zhao, Yumin, Weifeng Gui, Yishu Zhang, Gang Mo, Dayu Li, and Shigui Chong. "Inhibitory Effect of Ionizing Radiation on Echinococcus granulosus Hydatid Cyst." Diseases 7, no. 1 (February 18, 2019): 23. http://dx.doi.org/10.3390/diseases7010023.

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Background: Heavy ion radiation has more advantages than traditional radiation therapy in the treatment of cancer, mainly because of its superior biological effects. However, there is currently no reliable evidence that heavy ion radiation can induce cell death in hydatid cysts at the cellular and molecular level. In addition, we believe heavy ion therapy could be a potential alternative approach for the treatment of hydatid cysts. Methodology/Principal Finding: The hydatid cysts and protoscolices were obtained from an experimentally infected KunMing mice. LD50 was used to evaluate the death of the protoscolex. The cellular and ultrastructure of the parasites were observed under light and electron microscopes, the damage and copy numbers of mitochondrial DNA (mtDNA) were decided by QPCR. The apoptosis was evaluated by the expression and activity of caspase3. Dose-dependent ionizing radiation induced damage to the initial mtDNA. Echinococcosis cyst after ionizing radiation showed sparse cytoplasm, disorganized and clumped organelles, huge vacuoles, and villus deletions. The kinetic of DNA repair activity after X-ray irradiation was faster than those after carbon-ion irradiation. High doses of carbon ion radiation caused irreversible attenuation of mitochondrial DNA. Cysts showed obvious reduction in size after radiation. Carbon ion radiation was more effective than X-ray radiation in inhibiting hydatid cysts. Conclusions: These studies provide evidence that heavy-ion radiation can cause the extinction of hydatid cysts in vitro. The carbon-ion radiation is more advantageous than X-ray radiation in suppress hydatid cyst.

18

E. Prieto, L. X. Hallado, A. Guerrero, I. Álvarez, and C. Cisneros. "Effect of Laser Radiation on Biomolecules." Journal of Nuclear Physics, Material Sciences, Radiation and Applications 7, no. 2 (February 28, 2020): 123–28. http://dx.doi.org/10.15415/jnp.2020.72015.

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Time of flight laser photoionization has been used to study the response of some molecules of biological interest under laser radiation. One of the questions of great interest today is the effect of radiation on DNA and RNA molecules. Damage to these molecules can be caused directly by radiation or indirectly by secondary electrons created by radiation. As response of the radiation field fragmentation process can occur producing different ions with kinetic energies of a few electron volts. In this paper we present the results of the interaction of 355nm laser with the nitrogen bases adenine(A) and uracil(U) using time-of-flight spectrometry and the comparison of experimental results on the effects of laser radiation in (A) and (U) belonging to two different ring groups, purines and pyrimidines respectively,which are linked to form the AU pair of the RNA.

19

Symons, Martyn C. R. "Radiation effects in biological systems." Proceedings of the Royal Society of Edinburgh. Section B. Biological Sciences 102 (1994): 81–96. http://dx.doi.org/10.1017/s0269727000014007.

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SynopsisThis paper presents a chemist's view of the action of ionising radiation on matter with a range of simple examples. Attention is given to the ways in which electron spin resonance spectroscopy (which is described briefly) can be harnessed to give useful information about the initial stages of radiation damage. The effects of radiation are generally indiscriminate and hence damage to water is of special importance in biological systems. Water-derived free radicals will attack biomolecules (the indirect effect) and this mechanism is compared with direct damage events. Also, examples are given of some remarkably discriminate radiation-induced reactions.Specific attention is given to radiation-induced damage to proteins, and especially to aqueous DNA and DNA in chromatin and in cells. The importance of DNA strand-breaks is discussed in relation to both the production of mutations and cell death.

20

Gürsoy, Mehtap. "The Effect of Increased UV-B Radiation on the Terrestrial Ecosystem." Turkish Journal of Agriculture - Food Science and Technology 7, no. 8 (August 9, 2019): 1173. http://dx.doi.org/10.24925/turjaf.v7i8.1173-1176.2519.

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Against rapidly developing industry and increasing population, natural resources on earth are getting destroyed. One of the most important adverse effects on the environment is perhaps the depletion of ozone layer which protects the earth from harmful effects of UV radiation, especially UV-B. The effect of UV-B radiation can vary according to species. At high rates of UV-B radiation, many disorders in DNA, photosynthesis, morphological and physiological structure, and biomass accumulation in plants are observed. In this review, the effects of high UV-B radiation on terrestrial ecosystem are discussed.

21

Craig, Daniel J., Nisha S. Nanavaty, Monika Devanaboyina, Laura Stanbery, Danae Hamouda, Gerald Edelman, Lance Dworkin, and John J. Nemunaitis. "The abscopal effect of radiation therapy." Future Oncology 17, no. 13 (May 2021): 1683–94. http://dx.doi.org/10.2217/fon-2020-0994.

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Radiation therapy (RT) in some cases results in a systemic anticancer response known as the abscopal effect. Multiple hypotheses support the role of immune activation initiated by RT-induced DNA damage. Optimal radiation dose is necessary to promote the cGAS-STING pathway in response to radiation and initiate an IFN-1 signaling cascade that promotes the maturation and migration of dendritic cells to facilitate antigen presentation and stimulation of cytotoxic T cells. T cells then exert a targeted response throughout the body at areas not subjected to RT. These effects are further augmented through the use of immunotherapeutic drugs resulting in increased T-cell activity. Tumor-infiltrating lymphocyte presence and TREX1, KPNA2 and p53 signal expression are being explored as prognostic biomarkers.

22

Kong, FuQuan, Xiao Wang, MeiNan Ni, Li Sui, MingJian Yang та Kui Zhao. "The DNA concentration effect on DNA radiation damage induced by 7Li ions and γ rays". Science Bulletin 53, № 18 (вересень 2008): 2758–63. http://dx.doi.org/10.1007/s11434-008-0320-7.

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23

Bolsunovsky, A. Ya, D. V. Dementyev, T. S. Frolova, E. A. Trofimova, E. M. Iniatkina, S. A. Vasilyev, and O. I. Sinitsyna. "Effects of gamma-radiation on DNA damage in onion (Allium cepa L.) seedlings." Доклады Академии наук 489, no. 2 (November 20, 2019): 199–204. http://dx.doi.org/10.31857/s0869-56524892199-204.

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The effect of -radiation on the level of nuclear DNA damage in onion seedlings (Allium-test) was studied using the comet assay. DNA breaks were first found in cells of onion seedlings exposed to low-dose radiation ( 0,1 Gy). Dose dependence of DNA damage parameters showed nonlinear behavior: a linear section in the low-dose region (below 0,1 Gy) and a dose-independent plateau in the dose range between 1 and 5 Gy. Thus, the comet assay can be used to estimate the biological effects of low-dose gamma-radiation on Allium cepa seedlings.

24

Araújo, Maria Cristina P., Francisca da Luz Dias, Andréa O. Cecchi, Lusânia M. G. Antunes, and Catarina S. Takahashi. "Chromosome damage induced by DNA topoisomerase II inhibitors combined with g-radiation in vitro." Genetics and Molecular Biology 21, no. 3 (September 1998): 407–17. http://dx.doi.org/10.1590/s1415-47571998000300021.

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Combined radiation and antineoplastic drug treatment have important applications in cancer therapy. In the present work, an evaluation was made of two known topoisomerase II inhibitors, doxorubicin (DXR) and mitoxantrone (MXN), with g-radiation. The effects of DXR or MXN on g-radiation-induced chromosome aberrations in Chinese hamster ovary (CHO) cells were analyzed. Two concentrations of each drug, 0.5 and 1.0 µg/ml DXR, and 0.02 and 0.04 µg/ml MXN, were applied in combination with two doses of g-radiation (20 and 40 cGy). A significant potentiating effect on chromosomal aberrations was observed in CHO cells exposed to 1.0 µg/ml DXR plus 40 cGy. In the other tests, the combination of g-radiation with DXR or MXN gave approximately additive effects. Reduced mitotic indices reflected higher toxicity of the drugs when combined with radiation.

25

Springer, Mark S., and John A. W. Kirsch. "DNA Hybridization, the Compression Effect, and the Radiation of Diprotodontian Marsupials." Systematic Zoology 40, no. 2 (June 1991): 131. http://dx.doi.org/10.2307/2992253.

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26

Lafleur, M. V. M., E. J. Pluumackers-Westmuze, and H. Loman. "Effect of radiation-induced reduction of nitroimidazoles on biologically active DNA." International Journal of Radiation Oncology*Biology*Physics 12, no. 7 (July 1986): 1211–14. http://dx.doi.org/10.1016/0360-3016(86)90260-9.

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27

Demonchy, M., and M. Terrissol. "Simulation of radiation effect in DNA. Influence of the hydration shell." Journal de Chimie Physique 94 (1997): 296–99. http://dx.doi.org/10.1051/jcp/1997940296.

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28

Arkhangelskaya, E. Yu, N. Yu Vorobyeva, S. V. Leonov, A. N. Osipov, and A. L. Buchachenko. "Magnetic Isotope Effect on the Repair of Radiation-Induced DNA Damage." Russian Journal of Physical Chemistry B 14, no. 2 (March 2020): 314–17. http://dx.doi.org/10.1134/s1990793120020177.

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29

Horan, Annamarie D., Albert R. Giandomenico, and Cameron J. Koch. "Effect of Oxygen on Radiation-Induced DNA Damage in Isolated Nuclei." Radiation Research 152, no. 2 (August 1999): 144. http://dx.doi.org/10.2307/3580087.

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30

Springer, M. S., and J. A. W. Kirsch. "DNA Hybridization, the Compression Effect, and the Radiation of Diprotodontian Marsupials." Systematic Biology 40, no. 2 (June 1, 1991): 131–51. http://dx.doi.org/10.1093/sysbio/40.2.131.

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31

Alizadeh, Elahe, Ana G. Sanz, Gustavo García, and Léon Sanche. "Radiation Damage to DNA: The Indirect Effect of Low-Energy Electrons." Journal of Physical Chemistry Letters 4, no. 5 (February 25, 2013): 820–25. http://dx.doi.org/10.1021/jz4000998.

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32

Havaki, Sophia, Athanassios Kotsinas, Efstathios Chronopoulos, Dimitris Kletsas, Alexandros Georgakilas, and Vassilis G. Gorgoulis. "The role of oxidative DNA damage in radiation induced bystander effect." Cancer Letters 356, no. 1 (January 2015): 43–51. http://dx.doi.org/10.1016/j.canlet.2014.01.023.

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Wakayama, Sayaka, Daiyu Ito, Yuko Kamada, Toru Shimazu, Tomomi Suzuki, Aiko Nagamatsu, Ryoko Araki, et al. "Evaluating the long-term effect of space radiation on the reproductive normality of mammalian sperm preserved on the International Space Station." Science Advances 7, no. 24 (June 2021): eabg5554. http://dx.doi.org/10.1126/sciadv.abg5554.

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Space radiation may cause DNA damage to cells and concern for the inheritance of mutations in offspring after deep space exploration. However, there is no way to study the long-term effects of space radiation using biological materials. Here, we developed a method to evaluate the biological effect of space radiation and examined the reproductive potential of mouse freeze-dried spermatozoa stored on the International Space Station (ISS) for the longest period in biological research. The space radiation did not affect sperm DNA or fertility after preservation on ISS, and many genetically normal offspring were obtained without reducing the success rate compared to the ground-preserved control. The results of ground x-ray experiments showed that sperm can be stored for more than 200 years in space. These results suggest that the effect of deep space radiation on mammalian reproduction can be evaluated using spermatozoa, even without being monitored by astronauts in Gateway.

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Vasan, SS, and Srinivas Belur Veerachari. "Mobile Phone Electromagnetic Waves and Its Effect on Human Ejaculated Semen: An in vitro Study." International Journal of Infertility & Fetal Medicine 3, no. 1 (2012): 15–21. http://dx.doi.org/10.5005/jp-journals-10016-1034.

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ABSTRACT Mobile phones usage has seen an exponential growth recently. With this increasing demand, the amount of electromagnetic radiation (EMR) exposed is also increasing. Hence, we studied the effect of these radiations on ejaculated human semen and speculate the contribution of these harmful radiations in male infertility. Samples exposed to EMR showed a significant decrease in sperm motility and viability, increase in reactive oxygen species (ROS) and DNA fragmentation index (DFI) compared to unexposed group. We concluded that mobile phones emit electromagnetic waves which lead to oxidative stress in human semen and also cause changes in DNA fragmentation. We extrapolate these findings to speculate that these radiations may negatively affect spermatozoa and impair male fertility. How to cite this article Veerachari SB, Vasan SS. Mobile Phone Electromagnetic Waves and Its Effect on Human Ejaculated Semen: An in vitro Study. Int J Infertility Fetal Med 2012;3(1):15-21.

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Babayan, Nelly, Galina Hovhannisyan, Bagrat Grigoryan, Ruzanna Grigoryan, Natalia Sarkisyan, Gohar Tsakanova, Samvel Haroutiunian, and Rouben Aroutiounian. "Dose-rate effect of ultrashort electron beam radiation on DNA damage and repair in vitro." Journal of Radiation Research 58, no. 6 (September 12, 2017): 894–97. http://dx.doi.org/10.1093/jrr/rrx035.

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Abstract Laser-generated electron beams are distinguished from conventional accelerated particles by ultrashort beam pulses in the femtoseconds to picoseconds duration range, and their application may elucidate primary radiobiological effects. The aim of the present study was to determine the dose-rate effect of laser-generated ultrashort pulses of 4 MeV electron beam radiation on DNA damage and repair in human cells. The dose rate was increased via changing the pulse repetition frequency, without increasing the electron energy. The human chronic myeloid leukemia K-562 cell line was used to estimate the DNA damage and repair after irradiation, via the comet assay. A distribution analysis of the DNA damage was performed. The same mean level of initial DNA damages was observed at low (3.6 Gy/min) and high (36 Gy/min) dose-rate irradiation. In the case of low-dose-rate irradiation, the detected DNA damages were completely repairable, whereas the high-dose-rate irradiation demonstrated a lower level of reparability. The distribution analysis of initial DNA damages after high-dose-rate irradiation revealed a shift towards higher amounts of damage and a broadening in distribution. Thus, increasing the dose rate via changing the pulse frequency of ultrafast electrons leads to an increase in the complexity of DNA damages, with a consequent decrease in their reparability. Since the application of an ultrashort pulsed electron beam permits us to describe the primary radiobiological effects, it can be assumed that the observed dose-rate effect on DNA damage/repair is mainly caused by primary lesions appearing at the moment of irradiation.

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IJff, Marloes, Bregje van Oorschot, Arlene L. Oei, Przemek M. Krawczyk, Hans M. Rodermond, Lukas J. A. Stalpers, H. Petra Kok, Johannes Crezee, and Nicolaas A. P. Franken. "Enhancement of Radiation Effectiveness in Cervical Cancer Cells by Combining Ionizing Radiation with Hyperthermia and Molecular Targeting Agents." International Journal of Molecular Sciences 19, no. 8 (August 16, 2018): 2420. http://dx.doi.org/10.3390/ijms19082420.

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Hyperthermia (HT) and molecular targeting agents can be used to enhance the effect of radiotherapy (RT). The purpose of this paper is to evaluate radiation sensitization by HT and different molecular targeting agents (Poly [ADP-ribose] polymerase 1 inhibitor, PARP1-i; DNA-dependent protein kinase catalytic subunit inhibitor, DNA-PKcs-i and Heat Shock Protein 90 inhibitor, HSP90-i) in cervical cancer cell lines. Survival curves of SiHa and HeLa cells, concerning the combined effects of radiation with hyperthermia and PARP1-i, DNA-PKcs-i or HSP90-i, were analyzed using the linear-quadratic model: S(D)/S(0) = exp − (αD + βD2). The values of the linear-quadratic (LQ) parameters α and β, determine the effectiveness at low and high doses, respectively. The effects of these sensitizing agents on the LQ parameters are compared to evaluate dose-dependent differences in radio enhancement. Combination of radiation with hyperthermia, PARP1-i and DNA-PKcs-i significantly increased the value of the linear parameter α. Both α and β were significantly increased for HSP90-i combined with hyperthermia in HeLa cells, though not in SiHa cells. The Homologous Recombination pathway is inhibited by hyperthermia. When hyperthermia is combined with DNA-PKcs-i and PARP1-i, the Non-Homologous End Joining or Alternative Non-Homologous End Joining pathway is also inhibited, leading to a more potent radio enhancement. The observed increments of the α value imply that significant radio enhancement is obtained at clinically-used radiotherapy doses. Furthermore, the sensitizing effects of hyperthermia can be even further enhanced when combined with other molecular targeting agents.

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Hirano, Shin-ichi, Yusuke Ichikawa, Bunpei Sato, Haru Yamamoto, Yoshiyasu Takefuji, and Fumitake Satoh. "Molecular Hydrogen as a Potential Clinically Applicable Radioprotective Agent." International Journal of Molecular Sciences 22, no. 9 (April 27, 2021): 4566. http://dx.doi.org/10.3390/ijms22094566.

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Although ionizing radiation (radiation) is commonly used for medical diagnosis and cancer treatment, radiation-induced damages cannot be avoided. Such damages can be classified into direct and indirect damages, caused by the direct absorption of radiation energy into DNA and by free radicals, such as hydroxyl radicals (•OH), generated in the process of water radiolysis. More specifically, radiation damage concerns not only direct damages to DNA, but also secondary damages to non-DNA targets, because low-dose radiation damage is mainly caused by these indirect effects. Molecular hydrogen (H2) has the potential to be a radioprotective agent because it can selectively scavenge •OH, a reactive oxygen species with strong oxidizing power. Animal experiments and clinical trials have reported that H2 exhibits a highly safe radioprotective effect. This paper reviews previously reported radioprotective effects of H2 and discusses the mechanisms of H2, not only as an antioxidant, but also in intracellular responses including anti-inflammation, anti-apoptosis, and the regulation of gene expression. In doing so, we demonstrate the prospects of H2 as a novel and clinically applicable radioprotective agent.

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Korolev, V. G. "Molecular bases of the effect of low doses of radiation." Marine Biological Journal 5, no. 3 (September 30, 2020): 23–29. http://dx.doi.org/10.21072/mbj.2020.05.3.03.

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By definition, low doses are minimum doses of a damaging agent, in particular radiation, causing a recorded biological effect. The problem of exposure to low doses of radiation is being discussed in scientific literature for decades, but there is still no generally accepted conclusion concerning the existence of some features of the effect of low doses in contrast to that of acute exposure. This is due to the fact as follows: if being fixed, these effects have a weak expression and can be easily criticized. The second important aspect of this problem is that biological effects are mainly described phenomenologically in literature, without deciphering their molecular causes. In recent years, a number of articles appeared in which the authors, when studying exposure to low doses of DNA-tropic agents, show that postreplication repair (in particular, its error-free branch) plays a key role in these effects. In the laboratory of eukaryotic genetics of Petersburg Nuclear Physics Institute named by B. P. Konstantinov, it was possible to isolate unique yeast mutants with a disrupted branch of error-free postreplication repair. A study of the processes of eliminating DNA damage with minimal deviations of their number from a spontaneous level made it possible to explain at the molecular level the differences in cell response to low doses from acute exposure.

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Permadi, Wiryawan, Hanom Husni Syam, Hartanto Bayuaji, Tita Husnitawati Madjid, and Bayu Irsyad. "Securinega leucopyrus The Effect of Mobile Phone Radiation on Sperm DNA Fragmentation." International Journal of PharmTech Research 12, no. 03 (2019): 01–07. http://dx.doi.org/10.20902/ijptr.2019.120301.

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Schulte-Frohlinde, Dietrich. "The Effect of Oxygen and Thiols on the Radiation Damage of DNA." Free Radical Research Communications 6, no. 2-3 (January 1989): 181–83. http://dx.doi.org/10.3109/10715768909073465.

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41

Koo, Kwang Min, Sera Jung, Jin-Baek Kim, Sang Hoon Kim, Soon Jae Kwon, Won-Joong Jeong, Gook Hyun Chung, Si-Yong Kang, Yoon-E. Choi, and Joon-Woo Ahn. "Effect of ionizing radiation on the DNA damage response in Chlamydomonas reinhardtii." Genes & Genomics 39, no. 1 (October 17, 2016): 63–75. http://dx.doi.org/10.1007/s13258-016-0472-9.

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42

MASUDA, TAKAHIRO. "Radiation-chemical Discussion on Inverse Dose-rate Effect Observed in Radiation-induced Strand Breaks of Plasmid DNA." Journal of Radiation Research 35, no. 3 (1994): 157–67. http://dx.doi.org/10.1269/jrr.35.157.

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Takeoka, M., W. F. Ward, H. Pollack, D. W. Kamp, and R. J. Panos. "KGF facilitates repair of radiation-induced DNA damage in alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (June 1, 1997): L1174—L1180. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1174.

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Administration of exogenous keratinocyte growth factor (KGF) prevents or attenuates several forms of oxidant-mediated lung injury. Because DNA damage in epithelial cells is a component of radiation pneumotoxicity, we determined whether KGF ameliorated DNA strand breaks in irradiated A549 cells. Cells were exposed to 137Cs gamma rays, and DNA damage was measured by alkaline unwinding and ethidium bromide fluorescence after a 30-min recovery period. Radiation induced a dose-dependent increase in DNA strand breaks. The percentage of double-stranded DNA after exposure to 30 Gy increased from 44.6 +/- 3.5% in untreated control cells to 61.6 +/- 5.0% in cells cultured with 100 ng/ml KGF for 24 h (P < 0.05). No reduction in DNA damage occurred when the cells were cultured with KGF but maintained at 0 degree C during and after irradiation. The sparing effect of KGF on radiation-induced DNA damage was blocked by aphidicolin, an inhibitor of DNA polymerases-alpha, -delta, and -epsilon and by butylphenyl dGTP, which blocks DNA polymerase-alpha strongly and polymerases-delta and -epsilon less effectively. However, dideoxythymidine triphosphate, a specific inhibitor of DNA polymerase-beta, did not abrogate the KGF effect. Thus KGF increases DNA repair capacity in irradiated pulmonary epithelial cells, an effect mediated at least in part by DNA polymerases-alpha, -delta, and -epsilon. Enhancement of DNA repair capability after cell damage may be one mechanism by which KGF is able to ameliorate oxidant-mediated alveolar epithelial injury.

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Chegeni, N., E. Kouhkan, A. Hussain, and M. Hassanvand. "The effect of the nucleus random location on the cellular S-values – Based on Geant4-DNA." Applied Radiation and Isotopes 168 (February 2021): 109427. http://dx.doi.org/10.1016/j.apradiso.2020.109427.

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Zhao, Hai Tian, Zhen Yu Wang, Cui Lin Cheng, Feng Ming Ma, Xin Yang, and Lei Yao. "UV Protective Effect of Anthocyanin Extract from Lonicera caerulea var. Edulis." Applied Mechanics and Materials 195-196 (August 2012): 1294–99. http://dx.doi.org/10.4028/www.scientific.net/amm.195-196.1294.

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In the present study, we investigated the protective effect of anthocyanin extract from Lonicera caerulea var. edulis (LCA) on UVC-induced lipid and protein peroxidation using lecithin and Bull Serum Albumin (BSA) in vitro model. We also investigated the protective effect of anthocyanin on UVC induced cell injury in Spleen lymphocytes of mouse via MTT and comet assays. Peroxidation of lecithin and BSA generated by exposure to UVC radiation was significantly decreased by addition with various concentrations of LCA. Moreover, LCA exhibited an inhibitory effect on DNA damage induced by UVC radiation when compared with the control group, the DNA damage decrease at the LCA concentration of 50-200ug/ml, in comet assay. These results indicate that LCA has certain protective effect to ultraviolet radiation damage.

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Vo Thi, Thuong Lan, Ba Tuan Dinh, Bich Thuan Ta, Bang Diep Tran, and Minh Quynh Tran. "UV light induced DNA damages and the radiation protection effects of Lingzi mushrom extract." Nuclear Science and Technology 6, no. 3 (September 30, 2016): 40–47. http://dx.doi.org/10.53747/jnst.v6i3.166.

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UV light has strongly influenced on the growth of E. coli as well as caused DNA damages. Configurations of both genomic DNA and pUC 19 plasmids extracted from E. coli were significantly changed by the exposure to UV light of 254 nm and DLT, an extract of Ganoderma lucidum Lingzi mushroom. The results also revealed the radio-protective effects of DLT to UV radiation. By adding 2% DLT to its culturing suspension, the growth of E. coli was significantly decreased, whereas a low DLT amount of about 0.5% slightly improved its growth, indicated that the DLT extract can be used as a promising protective substance against UV radiation. At the molecular level, the radio-protective effects of DLT were observed for both UV treated DNA and protein. Thus, DLT can protect DNA in vivo, but not in vitro. This effect was also observed for Taq polymerase, suggested that the radio-protection effect of DLT may due to it accelerated the degradation of radicals or species that produced in the suspensions during UV exposure.

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Muzalov, I. I., and V. M. Mikhailenko. "PECULIARITIES OF DNA DAMAGE CAUSED BY EXOGENOUS NITRIC OXIDE COMBINED WITH FRACTIONATED LOW DOSE IONIZING RADIATION IN NORMAL AND TUMOR CELLS." Experimental Oncology 37, no. 1 (March 22, 2015): 40–43. http://dx.doi.org/10.31768/2312-8852.2015.37(1):40-43.

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The aim of this study was to investigate the reaction of normal and tumor cells to genotoxic effect of widespread environmental factors — exogenous nitric oxides and ionizing radiation. Methods: The animals were treated with NO (125 mg/m3) and low dose ioni zing radiation (10 acute exposures with 0.1 Gy each). Genotoxicity was estimated in vivo in rats peripheral blood lymphocytes, bone marrow cells and tumor cells of Guerin carcinoma. DNA damages were assessed by alkaline single-cell gel electrophoresis. Results: Exogenous nitric oxides as well as irradiation caused significant increase of DNA damage in all types of investigated cells. The genotoxic effect increased in the order: peripheral blood lymphocytes < bone marrow cells < Guerin carcinoma cells. The greatest genotoxic effect was registered in Guerin carcinoma cells on terminal phase of tumor growth in rats exposed to NO and low dose ionizing radiation. Conclusions: Long-term exposure to common environmental factors (exogenous nitric oxides and ionizing radiation) capable to induce DNA damage in diffe rent cells. Severity of the genotoxic effect depends on cell type and nature of impacting factors. NO caused more significant DNA damage than low dose ionizing radiation but the highest level of DNA damage was observed after their joint action. Obtained results confirm the real threat of cancer risk increase under combined action of common environmental factors of different nature.

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Lafleur, M. V. M., and H. Loman. "Radiation damage to ?X174 DNA and biological effects." Radiation and Environmental Biophysics 25, no. 3 (September 1986): 159–73. http://dx.doi.org/10.1007/bf01221222.

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Gangopadhyay, Sudeshna, and Parimal Karmakar. "Cellular response to the combined effect of trifluoperazine and ionizing radiation: A molecular study." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e13533-e13533. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e13533.

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e13533 Background: It is known that some phenothiazines group of drugs have the potential to modulate ionizing radiation (IR) induced cellular damage. In our previous study, we have shown that Trifluoperazine (TFP), a phenothiazine derivative antipsychotic drug, modulate the effect of IR by inhibiting the IR induced DNA double strand break (DSB) repair, and raising the possibility of using TFP as an adjuvant to radiotherapy. In the present study we tried to explore the mechanism of IR induced DNA damage repair inhibition by TFP. Methods: Effect of TFP and IR on cell viability was determined by MTT assay. Study of possible signaling pathway leading to IR induced cell killing was checked using indirect immunolabeling and transfection. Results: It was observed that the use of TFP (2.5 µg/mL) reduces the LD50 from 13 Gy to 7.5 Gy. After transfecting the cells with GFP-tagged Ku80 plasmid, we have seen that in the gamma-irradiated cells, Ku80 was completely localized in the nucleus, indicating close association of Ku with the broken DNA ends. However, in the TFP (2.5 μg/mL) treated cells, Ku80 was retained in the cytoplasm after irradiation. Similarly, with indirect immunofluorescence experiments using antibody against DNA-PKcs, the catalytic component of DNA-PK, large bright dots of DNA-PKcs was present in the nucleus when cells were treated with IR alone. But, when the cells were irradiated in the presence of TFP, DNA-PKcs migrated to the nucleus partially, even after 4 h of irradiation. Conclusions: Thus, TFP prevents the trafficking of DNA-PK complex from cytoplasm to nucleus and thereby inhibits the DNA-PK mediated NHEJ. Taken together, our results suggest that TFP sequestered the DNA-PK complex, which is a major player in non homologous end joining (NHEJ) and enhance the effect of IR.

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Kumari N, Suchetha, and Madhu L.N. "EFFECT OF ELECTRON BEAM RADIATION ON HEMATOPOIETIC CELLS OF SWISS ALBINO MICE." Journal of Health and Allied Sciences NU 01, no. 01/03 (September 2011): 15–18. http://dx.doi.org/10.1055/s-0040-1703513.

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AbstractIonizing radiation which results in the free radical formation and it leads to damage of biological macromolecules such as DNA, proteins, lipids. 36 male Swiss albino mice were used for survival assay, to find out the lethal dose of Electron Beam Radiation. It was found to be 10Gy was the lethal dose for mice. Different dosages (4Gy, 6Gy and 8Gy) of electron beam radiation were used to study the micronucleus formation in irradiated mice. The results showed micronucleus formation will increase linearly with radiation dosage.