scholarly journals Mitigation of Iron Irradiation-Induced Genotoxicity and Genomic Instability by Postexposure Dietary Restriction in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Bing Wang ◽  
Takanori Katsube ◽  
Kaoru Tanaka ◽  
Masahiro Murakami ◽  
Mitsuru Nenoi
Keyword(s):  
Genomic Instability ◽  
Dietary Restriction ◽  
Initial Energy ◽  
Free Access ◽  
Nuclear Accidents ◽  
Iron Particles ◽  
High Let ◽  
Manned Space ◽  
Total Body ◽  
Underlying Mechanisms

Background and Purpose. Postexposure onset of dietary restriction (DR) is expected to provide therapeutic nutritional approaches to reduce health risk from exposure to ionizing radiation (IR) due to such as manned space exploration, radiotherapy, or nuclear accidents as IR could alleviate radiocarcinogenesis in animal models. However, the underlying mechanisms remain largely unknown. This study is aimed at investigating the effect from postexposure onset of DR on genotoxicity and genomic instability (GI) induced by total body irradiation (TBI) in mice. Materials and Methods. Mice were exposed to 2.0 Gy of accelerated iron particles with an initial energy of 500 MeV/nucleon and a linear energy transfer (LET) value of about 200 keV/μm. After TBI, mice were either allowed to free access to a standard laboratory chow or treated under DR (25% cut in diet). Using micronucleus frequency (MNF) in bone marrow erythrocytes, induction of acute genotoxicity and GI in the hematopoietic system was, respectively, determined 1 and 2 months after TBI. Results and Conclusions. TBI alone caused a significant increase in MNF while DR alone did not markedly influence the MNF. DR induced a significant decrease in MNF compared to the treatment by TBI alone. Results demonstrated that postexposure onset of DR could relieve the elevated MNF induced by TBI with high-LET iron particles. These findings indicated that reduction in acute genotoxicity and late GI may be at least a part of the mechanisms underlying decreased radiocarcinogenesis by DR.

scholarly journals What radiation dose for DLA-identical canine marrow grafts? [published erratum appears in Blood 1989 Feb;73(2):624]

Blood ◽  
1988 ◽  
Vol 72 (4) ◽  
pp. 1300-1304 ◽  
Author(s):  
R Storb ◽  
RF Raff ◽  
FR Appelbaum ◽  
FW Schuening ◽  
BM Sandmaier ◽  
...  
Keyword(s):  
Radiation Dose ◽  
Total Body Irradiation ◽  
Graft Rejection ◽  
Graft Failure ◽  
Canine Model ◽  
Radiation Doses ◽  
Nuclear Accidents ◽  
Total Body ◽  
Allogeneic Marrow ◽  
Marrow Cells

Abstract In view of reported attempts at marrow grafting after nuclear accidents with a broad range of radiation exposures, the present study explored the total-body irradiation (TBI) conditions needed for engraftment in a canine model by using marrow from DLA-identical littermates. Previous studies have shown that such grafts are consistently successful when recipients are exposed to 920 cGy of TBI delivered at a rate of 7 cGy/min from opposing dual cobalt sources. The present TBI doses were all in the lethal range. Five dogs were administered 450 cGy; seven dogs, 600 cGy; five dogs, 700 cGy; and five dogs, 800 cGy of TBI administered at 7 cGy/min. They received a median of 3.3 x 10(8) marrow cells/kg intravenously after completion of radiation. Results showed transient allogeneic marrow engraftment in all dogs administered the lowest dose of TBI studied (450 cGy). Importantly, transient grafts permitted four of five dogs to live long enough for autologous marrow recovery to occur. At increasing radiation doses, 600, 700, and 800 cGy, the risk of graft failure lessened, with 3 of 7, 2 of 5, and 1 of 5 dogs, respectively, showing graft rejection. Fewer dogs survived with autologous marrow recovery, and more showed sustained allogeneic engraftment (4 of 7, 3 of 5, and 4 of 5 dogs, respectively). We conclude that DLA-identical littermate marrow grafts are beneficial in the setting of otherwise lethal radiation exposures, with most dogs either experiencing sustained allogeneic engraftment or surviving with autologous marrow recovery due to the extended support provided by a transient allogeneic graft.

Bystander-mediated genomic instability after high LET radiation in murine primary haemopoietic stem cells

2006 ◽  
Vol 597 (1-2) ◽  
pp. 50-61 ◽  
Author(s):  
Deborah A. Bowler ◽  
Stephen R. Moore ◽  
Denise A. Macdonald ◽  
Sharon H. Smyth ◽  
Peter Clapham ◽  
...  
Keyword(s):  
Stem Cells ◽  
Genomic Instability ◽  
Haemopoietic Stem Cells ◽  
High Let Radiation ◽  
High Let

Changes in Bone Mineral Density Associated with Dietary-Induced Loss of Body Mass in Young Women

1994 ◽  
Vol 87 (3) ◽  
pp. 343-348 ◽  
Author(s):  
S. J. Ramsdale ◽  
E. J. Bassey
Keyword(s):  
Bone Mineral Density ◽  
Lumbar Spine ◽  
Body Mass ◽  
Bone Mineral ◽  
Dietary Restriction ◽  
Calcium Intake ◽  
Dietary Assessment ◽  
Premenopausal Women ◽  
Mineral Density ◽  
Total Body

1. Moderately overweight, premenopausal women were assessed for bone mineral density of the total body, lumbar spine and proximal femur before and after 6 months of modest dietary restriction (minimum 4800 kJ/day). The aim was to evaluate the effect of loss of body mass on bone mineral density. 2. Dietary assessment included two analyses of 3 day weighed food intakes, one before and the other after 4 months of dietary restriction. Energy and calcium intakes were significantly reduced by 27% and 5%, respectively. The change in calcium intake was negatively and significantly related to initial levels of calcium intake. 3. A significant mean loss of 3.4 ± 3.1 kg in body mass was achieved mainly in the first 3 months of the study; it was accompanied by significant losses at 6 months in bone mineral density in the total body of 0.7% and in the lumbar spine of 0.5%. There were no changes in the femur. 4. The change in bone mineral density in the total body was significantly related to the reduced absolute calcium intake, initial bone mineral density and loss of body mass. The change in bone mineral density in the spine was significantly related to the change in calcium intake. 5. These modest losses could be a threat in women with lower bone mineral density, and indicate the importance of maintaining a high intake of calcium during dietary restriction.

scholarly journals The potential role of epigenetic responses to diet in ageing

2011 ◽  
Vol 70 (3) ◽  
pp. 374-384 ◽  
Author(s):  
Dianne Ford ◽  
Laura J. Ions ◽  
Fatema Alatawi ◽  
Luisa A. Wakeling
Keyword(s):  
Dna Methylation ◽  
Life Course ◽  
Dietary Restriction ◽  
Later Life ◽  
Sirtuin 1 ◽  
Beneficial Effects ◽  
Epigenetic Effects ◽  
Underlying Mechanisms ◽  
Improve Health

Epigenetic changes may be causal in the ageing process and may be influenced by diet, providing opportunities to improve health in later life. The aim of this review is to provide an overview of several areas of research relevant to this topic and to explore a hypothesis relating to a possible role of epigenetic effects, mediated by sirtuin 1, in the beneficial effects of dietary restriction, including increased lifespan. Epigenetic features of ageing include changes in DNA methylation, both globally and at specific loci, which differ between individuals. A major focus of research on dietary influences on epigenetic status has been on nutrition in utero, because the epigenome is probably particularly malleable during this life-course window and because epigenetic marking by early exposures is a compelling mechanism underlying effects on lifelong health. We explore the potential of diet during adulthood, including the practice of dietary restriction, to affect the epigenetic architecture. We report progress with respect to deriving data to support our hypothesis that sirtuin 1 may mediate some of the effects of dietary restriction through effects on DNA methylation and note observations that resveratrol affects DNA methylation and other epigenetic features. Disentangling cause and effect in the context of epigenetic change and ageing is a challenge and requires better understanding of the underlying mechanisms and also the development of more refined experimental tools to manipulate the epigenetic architecture, to facilitate hypothesis-driven research to elucidate these links and thus to exploit them to improve health across the full life-course through dietary measures.

scholarly journals NADPH oxidase inhibition attenuates total body irradiation-induced haematopoietic genomic instability

Mutagenesis ◽  
2011 ◽  
Vol 26 (3) ◽  
pp. 431-435 ◽  
Author(s):  
S. K. Pazhanisamy ◽  
H. Li ◽  
Y. Wang ◽  
I. Batinic-Haberle ◽  
D. Zhou
Keyword(s):  
Nadph Oxidase ◽  
Genomic Instability ◽  
Total Body Irradiation ◽  
Oxidase Inhibition ◽  
Nadph Oxidase Inhibition ◽  
Total Body

scholarly journals MicroRNAs Responding to Space Radiation

2020 ◽  
Vol 21 (18) ◽  
pp. 6603
Author(s):  
Yujie Yan ◽  
Kunlan Zhang ◽  
Guangming Zhou ◽  
Wentao Hu
Keyword(s):  
Radiation Risk ◽  
Space Radiation ◽  
High Energy ◽  
Atom Number ◽  
Potential Threat ◽  
Functional Studies ◽  
Deep Space Exploration ◽  
Biological Responses ◽  
High Let ◽  
Underlying Mechanisms

High-energy and high-atom-number (HZE) space radiation poses an inevitable potential threat to astronauts on deep space exploration missions. Compared with low-LET radiation, high-energy and high-LET radiation in space is more efficient in inducing clustered DNA damage with more serious biological consequences, such as carcinogenesis, central nervous system injury and degenerative disease. Space radiation also causes epigenetic changes in addition to inducing damage at the DNA level. Considering the important roles of microRNAs in the regulation of biological responses of radiation, we systematically reviewed both expression profiling and functional studies relating to microRNAs responding to space radiation as well as to space compound environment. Finally, the directions for improvement of the research related to microRNAs responding to space radiation are proposed. A better understanding of the functions and underlying mechanisms of the microRNAs responding to space radiation is of significance to both space radiation risk assessment and therapy development for lesions caused by space radiation.

Genomic instability in cultured stem cells: associated risks and underlying mechanisms

2011 ◽  
Vol 6 (5) ◽  
pp. 653-662 ◽  
Author(s):  
Andrew L Ross ◽  
Daniel E Leder ◽  
Jonathan Weiss ◽  
Jan Izakovic ◽  
James M Grichnik
Keyword(s):  
Stem Cells ◽  
Genomic Instability ◽  
Underlying Mechanisms
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