DNA data storage is a potential alternative to magnetic tape for archival storage purposes, promising substantial gains in information density. Critical to the success of DNA as a storage media is an understanding of the role of environmental factors on the longevity of the stored information. In this paper, we evaluate the effect of exposure to ionizing particle radiation, a cause of data loss in traditional magnetic media, on the longevity of data in DNA data storage pools. We develop a mass action kinetics model to estimate the rate of damage accumulation in DNA strands due to neutron interactions with both nucleotides and residual water molecules, then utilize the model to evaluate the effect several design parameters of a typical DNA data storage scheme have on expected data longevity. Finally, we experimentally validate our model by exposing dried DNA samples to different levels of neutron irradiation and analyzing the resulting error profile. Our results show that particle radiation is not a significant contributor to data loss in DNA data storage pools under typical storage conditions.

Biological effects induced by diverse types of ionizing radiation are known to show important variations. Nanodosimetry is suitable for studying the link between these variations and the patterns of radiation interactions within nanometer-scale volumes, using experimental techniques complemented by Monte Carlo track structure (MCTS) simulations. However, predicted nanodosimetric quantities differ among MCTS codes, primarily because each code employs distinct molecular-scale particle interaction models. This multi-code study examines these variations for low-energy electrons (20-10,000 eV), which play a critical role in energy deposition and biological effects by virtually all types of ionizing radiation. Specifically, the hypothesis tested in this work is that inter-code variability in nanodosimetry results is mainly caused by differences in assumptions regarding total interaction cross sections. Ionization cluster size distributions and derived nanodosimetric parameters were simulated with seven MCTS codes (PARTRAC, PHITS-TS, MCwater, PTra, and three Geant4-DNA options) in liquid water as a surrogate for biological tissue. Significant inter-code differences were observed, especially at the lowest energies. They were substantially reduced upon replacing the original cross sections in each code with a common, averaged dataset, created ad-hoc for this study and not based on theoretical assumptions. For example, for 50 eV electrons in 8 nm spheres, the variability in the predict

Mechanistic modeling of DNA double strand break (DSB) rejoining is important for quantifying and medically exploiting radiation-induced cytotoxicity (e.g. in cancer radiotherapy). Most radiation-induced DSBs are quickly-rejoinable and are rejoined within the first 1-2 hours after irradiation. Others are slowly-rejoinable (persist for several hours), and yet others are essentially unrejoinable (persist for >24 hours). The dependences of DSB rejoining kinetics on radiation dose and dose rate remain incompletely understood. We hypothesize that the fraction of slowly-rejoinable and/or unrejoinable DSBs increases with increasing dose/dose rate. This radiation-dependent (RD) model was implemented using differential equations for three DSB classes: quickly-rejoinable, slowly-rejoinable and unrejoinable. Radiation converts quickly-rejoinable to slowly-rejoinable, and slowly-rejoinable to unrejoinable DSBs. We used large published data sets on DSB rejoining in yeast exposed to sparsely-ionizing (electrons and γ-rays, single or split-doses, high or low dose rates) and densely-ionizing (α-particles) radiation to compare the performances of the proposed RD formalism and the established two-lesion kinetic (TLK) model. These yeast DSB rejoining data were measured within the radiation dose range relevant for clonogenic cell survival, whereas in mammalian cells DSB rejoining is usually measured only at supra-lethal doses for technical reasons. The RD model described both sparsely-ionizing an

Abstract Background Ionizing radiation (IR) is high-energy radiation that has the potential to displace electrons from atoms and break chemical bonds. It has the ability to introduce mutations, DNA strand breakage, and cell death. Being a radiosensitive organ, exposure of the thyroid gland to IR can lead to significant changes in its function. Aim of the work Was to measure the levels of thyroid hormones panel and ultrasonography abnormalities in medical staff occupationally exposed to IR. Subjects and methods A total of 120 subjects were divided into three main groups: Group I: radiation-exposed workers occupationally exposed to radioiodine (131I) (n = 40), Group II: radiation-exposed workers occupationally exposed to X-ray (n = 40), and Group III: non-exposed healthy professionals matched in age and sex with the previous groups (n = 40). Thyroid hormones panel including free triiodothyronine (fT3), free thyroxine (fT4), thyroid-stimulating hormone (TSH), anti-thyroperoxidase antibodies (anti-TPO), and thyroglobulin (Tg) were measured. Thyroid ultrasonography was performed. Oxidative stress markers such as malondialdehyde (MDA), hydrogen peroxide (H2O2), and total antioxidant capacity (TAC) were measured. Results Group I had significantly higher fT3 levels than the control group. fT3 levels were considerably higher, while TSH was substantially lower in group II participants than in the control group. Tg was markedly lower in radiation-exposed workers. However, anti-TPO level

Abstract Experiments have shown that non-double strand break (DSB) clustered damage consisting of two or more base damages (BDs) or BD with single strand breaks (SSBs) occur with higher frequency than DSBs after ionizing radiation exposure. However experiments that measure tandem non-DSB clusters have not been developed. I develop a probability model of clustered damage that is combined with energy imparted spectra to predict the relative contributions of tandem and bistranded non-DSB clustered damage. The model considers probabilities for direct damage to sugar-phosphate moieties leading to SSBs, direct damage to DNA bases leading to abasic or oxidized sites, and indirect damage leading to radical formation with subsequent SSB and BD formation. Additional probabilities account for relative location of SSB and BD to model damage clusters. The model predicts for electrons and ions the relative contribution of tandem or bistranded lesions, the larger occurrence of clustered non-DSBs compared to DSBs, and the predominance of mixtures of damage types. Predictions of ratios of non-DSB clusters to DSB of 4-to-6 are found for electrons and high energy ions. The model provides an accurate method to predict DSB and non-DSB damage clusters as a function of radiation modality and to model resulting damage processing.