Feeding mice palm carotene prevents DNA damage in bone marrow and reduction of peripheral leukocyte counts, and enhances survival following X-ray irradiation

SummaryGaucher disease is the most prevalent inherited, lysosomal storage disease and is caused by deficient activity of the enzyme β-glucocerebrosidase. Bone and bone marrow alterations are frequent in the most prevalent non-neuronopathic form of Gaucher disease. Imaging of bone manifestations in Gaucher disease is performed by a variety of imaging methods, conventional X-ray and MRI as the most frequently and most important ones. However, different modalities of scintigraphic imaging have also been used. This article gives an overview on scintigraphic imaging with respect to bone manifestations in Gaucher disease discussing the advantages and limitations of scintigraphic imaging in comparison to other imaging methods.

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Intracellular Generation of Reactive Oxygen Species and DNA Damage in Escherichia Coli Mutants Exposed to Electromagnetic Field and X-Ray

Environmental Technology ◽

10.1080/09593332008616791 ◽

1999 ◽

Vol 20 (1) ◽

pp. 45-51 ◽

Cited By ~ 1

Author(s):

Y. Yonezawa ◽

J. Miyakoshi ◽

H. Takebe ◽

H. Nishioka

Keyword(s):

Escherichia Coli ◽

Reactive Oxygen Species ◽

Dna Damage ◽

Electromagnetic Field ◽

Reactive Oxygen ◽

Oxygen Species ◽

X Ray

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Exposure of the cytoplasm to low-dose X-rays modifies ataxia telangiectasia mutated-mediated DNA damage responses

Scientific Reports ◽

10.1038/s41598-021-92213-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Munetoshi Maeda ◽

Masanori Tomita ◽

Mika Maeda ◽

Hideki Matsumoto ◽

Noriko Usami ◽

...

Keyword(s):

Dna Damage ◽

Cell Death ◽

Ataxia Telangiectasia ◽

Kinase Inhibitor ◽

Surrogate Marker ◽

X Rays ◽

Ataxia Telangiectasia Mutated ◽

Whole Cell ◽

X Ray ◽

Dna Damage Responses

AbstractWe recently showed that when a low X-ray dose is used, cell death is enhanced in nucleus-irradiated compared with whole-cell-irradiated cells; however, the role of the cytoplasm remains unclear. Here, we show changes in the DNA damage responses with or without X-ray microbeam irradiation of the cytoplasm. Phosphorylated histone H2AX foci, a surrogate marker for DNA double-strand breaks, in V79 and WI-38 cells are not observed in nucleus irradiations at ≤ 2 Gy, whereas they are observed in whole-cell irradiations. Addition of an ataxia telangiectasia mutated (ATM) kinase inhibitor to whole-cell irradiations suppresses foci formation at ≤ 2 Gy. ABL1 and p73 expression is upregulated following nucleus irradiation, suggesting the induction of p73-dependent cell death. Furthermore, CDKN1A (p21) is upregulated following whole-cell irradiation, indicating the induction of cell cycle arrest. These data reveal that cytoplasmic radioresponses modify ATM-mediated DNA damage responses and determine the fate of cells irradiated at low doses.

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In situ monitoring of the influence of water on DNA radiation damage by near-ambient pressure X-ray photoelectron spectroscopy

Communications Chemistry ◽

10.1038/s42004-021-00487-1 ◽

2021 ◽

Vol 4 (1) ◽

Author(s):

Marc Benjamin Hahn ◽

Paul M. Dietrich ◽

Jörg Radnik

Keyword(s):

Dna Damage ◽

Radiation Damage ◽

Photoelectron Spectroscopy ◽

Ambient Pressure ◽

In Situ Monitoring ◽

Strong Increase ◽

Oh Radicals ◽

Strand Breaks ◽

X Ray

AbstractIonizing radiation damage to DNA plays a fundamental role in cancer therapy. X-ray photoelectron-spectroscopy (XPS) allows simultaneous irradiation and damage monitoring. Although water radiolysis is essential for radiation damage, all previous XPS studies were performed in vacuum. Here we present near-ambient-pressure XPS experiments to directly measure DNA damage under water atmosphere. They permit in-situ monitoring of the effects of radicals on fully hydrated double-stranded DNA. The results allow us to distinguish direct damage, by photons and secondary low-energy electrons (LEE), from damage by hydroxyl radicals or hydration induced modifications of damage pathways. The exposure of dry DNA to x-rays leads to strand-breaks at the sugar-phosphate backbone, while deoxyribose and nucleobases are less affected. In contrast, a strong increase of DNA damage is observed in water, where OH-radicals are produced. In consequence, base damage and base release become predominant, even though the number of strand-breaks increases further.

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Monitoring and treatment of MDS in genetically susceptible persons

Hematology ◽

10.1182/hematology.2019000020 ◽

2019 ◽

Vol 2019 (1) ◽

pp. 105-109 ◽

Cited By ~ 1

Author(s):

Stella M. Davies

Keyword(s):

Bone Marrow ◽

Dna Damage ◽

Bone Marrow Failure ◽

Treatment Strategies ◽

Informed Choice ◽

Dyskeratosis Congenita ◽

Careful Consideration ◽

Host Susceptibility ◽

Bone Marrow Failure Syndromes ◽

Severe Infections

Abstract Genetic susceptibility to myelodysplastic syndrome (MDS) occurs in children with inherited bone marrow failure syndromes, including Fanconi anemia, Shwachman Diamond syndrome, and dyskeratosis congenita. Available evidence (although not perfect) supports annual surveillance of the blood count and bone marrow in affected persons. Optimal treatment of MDS in these persons is most commonly transplantation. Careful consideration must be given to host susceptibility to DNA damage when selecting a transplant strategy, because significant dose reductions and avoidance of radiation are necessary. Transplantation before evolution to acute myeloid leukemia (AML) is optimal, because outcomes of AML are extremely poor. Children and adults can present with germline mutations in GATA2 and RUNX1, both of which are associated with a 30% to 40% chance of evolution to MDS. GATA2 deficiency may be associated with a clinically important degree of immune suppression, which can cause severe infections that can complicate transplant strategies. GATA2 and RUNX1 deficiency is not associated with host susceptibility to DNA damage, and therefore, conventional treatment strategies for MDS and AML can be used. RUNX1 deficiency has a highly variable phenotype, and MDS can occur in childhood and later in adulthood within the same families, making annual surveillance with marrow examination burdensome; however, such strategies should be discussed with affected persons, allowing an informed choice.

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X-ray and UV Radiation Damage of dsDNA/Protein Complexes

Molecules ◽

10.3390/molecules26113132 ◽

2021 ◽

Vol 26 (11) ◽

pp. 3132

Author(s):

Paweł Wityk ◽

Dorota Kostrzewa-Nowak ◽

Beata Krawczyk ◽

Michał Michalik ◽

Robert Nowak

Keyword(s):

Dna Damage ◽

Simple Model ◽

Uv Radiation ◽

Protein Complexes ◽

Chemical Processes ◽

Model Systems ◽

Degradation Pathways ◽

X Ray ◽

Physico Chemical ◽

Sensitization Process

Radiation and photodynamic therapies are used for cancer treatment by targeting DNA. However, efficiency is limited due to physico-chemical processes and the insensitivity of native nucleobases to damage. Thus, incorporation of radio- and photosensitizers into these therapies should increase both efficacy and the yield of DNA damage. To date, studies of sensitization processes have been performed on simple model systems, e.g., buffered solutions of dsDNA or sensitizers alone. To fully understand the sensitization processes and to be able to develop new efficient sensitizers in the future, well established model systems are necessary. In the cell environment, DNA tightly interacts with proteins and incorporating this interaction is necessary to fully understand the DNA sensitization process. In this work, we used dsDNA/protein complexes labeled with photo- and radiosensitizers and investigated degradation pathways using LC-MS and HPLC after X-ray or UV radiation.

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