Consumption of Apigenin Prevents Radiation-induced Gut Dysbiosis in Male C57BL/6J Mice Exposed to Silicon Ions.

The search for medical treatments to prevent radiation-induced damage to gastrointestinal tissue is crucial as such injuries can be fatal. This study aimed to investigate the effects of apigenin (AP) on the gut microbiome of irradiated mice, as it is a promising radiation countermeasure. Male C57BL/6J mice were divided into four groups, with six mice in each group.

Early- and late-occurring damage in bone marrow cells of male CBA/Ca mice exposed whole-body to 1 GeV/n Ti ions.

Purpose: To determine the early- and late-occurring damage in the bone marrow (BM) and peripheral blood cells of male CBA/Ca mice after exposure to 0, 0.1, 0.25, or 0.

Late Effects of Low-Dose Radiation on the Bone Marrow, Lung, and Testis Collected From the Same Exposed BALB/cJ Mice.

We used 3 biological metrics highly relevant to health risks, that is, cell death, inflammation, and global DNA methylation, to determine the late effects of low doses (0.05 or 0.1 Gy) of Cs γ rays on the bone marrow, lung, and testis collected at 6 months post-irradiation from the same exposed BALB/cJ mouse.

Persistent depletion of plasma gelsolin (pGSN) after exposure of mice to heavy silicon ions.

Little is known about plasma proteins that can be used as biomarkers for early and late responses to radiation. The purpose of this study was to determine a link between depletion of plasma gelsolin (pGSN) and cell-death as well as inflammatory responses in the lung (one of the tissues known to be radiosensitive) of the same exposed CBA/CaJ mice after exposure to heavy silicon (Si) ions. To prevent the development of multiple organ dysfunctions, pGSN (an important component of the extracellular actin-scavenging system) is responsible for the removal of actin that is released into the circulation during inflammation and from dying cells.

Effects of Medical Diagnostic Low-dose X Rays on Human Lymphocytes: Mitochondrial Membrane Potential, Apoptosis and Cell Cycle.

Low-dose radiation is widely used across the world for the diagnosis of many diseases by means of a variety of imaging technologies. However, the harmful effects of exposure to low-dose radiation during medical examination remain controversial. The authors studied the effects of medical diagnostic low-dose x rays (i.

Induction of Chronic Inflammation and Altered Levels of DNA Hydroxymethylation in Somatic and Germinal Tissues of CBA/CaJ Mice Exposed to (48)Ti Ions.

Although the lung is one of the target organs at risk for cancer induction from exposure to heavy ions found in space, information is insufficient on cellular/molecular responses linked to increased cancer risk. Knowledge of such events may aid in the development of new preventive measures. Furthermore, although it is known that germinal cells are sensitive to X- or γ-rays, there is little information on the effects of heavy ions on germinal cells.

Health Benefits of Exposure to Low-dose Radiation.

Although there is no doubt that exposure to high doses of radiation (delivered at a high dose-rate) induces harmful effects, the health risks and benefits of exposure to low levels (delivered at a low dose-rate) of toxic agents is still a challenging public health issue. There has been a considerable amount of published data against the linear no-threshold (LNT) model for assessing risk of cancers induced by radiation. The LNT model for risk assessment creates "radiophobia," which is a serious public health issue.

Late-occurring chromosome aberrations and global DNA methylation in hematopoietic stem/progenitor cells of CBA/CaJ mice exposed to silicon ((28)Si) ions.

Although myeloid leukemia (ML) is one of the major health concerns from exposure to space radiation, the risk prediction for developing ML is unsatisfactory. To increase the reliability of predicting ML risk, a much improved understanding of space radiation-induced changes in the target cells, i.e.

Proteomic Profiling of Hematopoietic Stem/Progenitor Cells after a Whole Body Exposure of CBA/CaJ Mice to Titanium (Ti) Ions.

Myeloid leukemia (ML) is one of the major health concerns from exposure to radiation. However, the risk assessment for developing ML after exposure to space radiation remains uncertain. To reduce the uncertainty in risk prediction for ML, a much increased understanding of space radiation-induced changes in the target cells, , hematopoietic stem/progenitor cells (HSPCs), is critically important.

Induction of chronic oxidative stress, chronic inflammation and aberrant patterns of DNA methylation in the liver of titanium-exposed CBA/CaJ mice.

Purpose: To investigate the biological effects of titanium ((48)Ti, one of the important heavy ions found in space) in the liver of exposed-mice.

Materials And Methods: We gave adult male CBA/CaJ mice a whole-body exposure to a total dose of 0, 0.1, 0.

Response to Baverstock, K. Comments on Rithidech, K.N.; et al. Lack of Genomic Instability in Bone Marrow Cells of SCID Mice Exposed Whole-Body to Low-Dose Radiation. Int. J. Environ. Res. Public Health 2013, 10, 1356-1377.

We thank Dr. Baverstock [1] for his interest in reading our article and his time in writing his comments for our work [2]. We, however, respectfully disagree with his statement that we made "two category errors" associated with the assessment of the occurrence of "genomic instability" by determining the frequencies of delayed- or late-occurring chromosomal damage.

Effects of 100MeV protons delivered at 0.5 or 1cGy/min on the in vivo induction of early and delayed chromosomal damage.

Little is known about in vivo cytogenetic effects of protons delivered at the dose and dose rates encountered in space. We determined the effects of 100MeV protons, one of the most abundant type of protons produced during solar particle events (SPE), on the induction of chromosome aberrations (CAs) in bone marrow (BM) cells collected at early (3 and 24h) and late (6 months) time-points from groups of BALB/cJ mice (a known radiosensitive strain) exposed whole-body to 0 (sham-controls), 0.5, or 1.

Persistence of apoptosis and inflammatory responses in the heart and bone marrow of mice following whole-body exposure to ²⁸Silicon (²⁸Si) ions.

It has been well established that the bone marrow (BM) is a radiosensitive tissue, but the radiosensitivity of the heart is poorly understood. In this study, we investigated the comparative effects of ²⁸Silicon (²⁸Si) ions (one type of heavy ion found in space) on tissue from the heart and the BM of exposed mice. We gave adult male CBA/CaJ mice a whole-body exposure to a total dose of 0, 0.

Lack of genomic instability in bone marrow cells of SCID mice exposed whole-body to low-dose radiation.

It is clear that high-dose radiation is harmful. However, despite extensive research, assessment of potential health-risks associated with exposure to low-dose radiation (at doses below or equal to 0.1 Gy) is still challenging.

Attenuation of oxidative damage and inflammatory responses by apigenin given to mice after irradiation.

We determined the in vivo efficacy of apigenin, as an anti-oxidant and anti-inflammatory agent, given to mice after irradiation. Various concentrations of apigenin (0, 10, 20, and 40mg/kg body weight) were administered to mice by a single intraperitoneal injection 3hr after receiving 0 or 3Gy of (137)Cs gamma rays. Mice receiving vehicle only (no radiation and no apigenin) served as sham controls.

No Evidence for the In Vivo Induction of Genomic Instability by Low Doses of CS Gamma Rays in Bone Marrow Cells of BALB/CJ and C57BL/6J Mice.

In spite of extensive research, assessment of potential health risks associated with exposure to low-dose (≤ 0.1 Gy) radiation is still challenging. We evaluated the in vivo induction of genomic instability, expressed as late-occurring chromosome aberrations, in bone-marrow cells of two strains of mouse with different genetic background, i.

Identification of proteins secreted into the medium by human lymphocytes irradiated in vitro with or without adaptive environments.

There is increasing evidence to support the hypothesis of adaptive response, a phenomenon in which protection arises from a low-dose radiation (<0.1 Gy) against damage induced by subsequent exposure to high-dose radiation. The molecular mechanisms underlying such protection are poorly understood.

Dose-rate effects of protons on in vivo activation of nuclear factor-kappa B and cytokines in mouse bone marrow cells.

The objective of this study was to determine the kinetics of nuclear factor-kappa B (NF-kappaB) activation and cytokine expression in bone marrow (BM) cells of exposed mice as a function of the dose rate of protons. The cytokines included in this study are pro-inflammatory [i.e.

Protein-expression profiles in mouse blood-plasma following acute whole-body exposure to (137)Cs gamma rays.

Purpose: To compare the pattern of protein-expression profiles in blood-plasma after exposure of CBA/CaJ mice to 0 or 3 Gy of (137)Cs gamma rays.

Materials And Methods: Two-dimensional electrophoresis gel coupled with mass spectrometry was used to analyze blood-samples collected at days 2 and 7 post-irradiation. At each sacrifice-time, alterations in expression-level of protein spots between control- and exposed-groups were analyzed statistically by the PDQuest software using Student's t-test (at the significance level of p < 0.

Evidence for radiation hormesis after in vitro exposure of human lymphocytes to low doses of ionizing radiation.

Previous research has demonstrated that adding a very small gamma-ray dose to a small alpha radiation dose can completely suppress lung cancer induction by alpha radiation (a gamma-ray hormetic effect). Here we investigated the possibility of gamma-ray hormesis during low-dose neutron irradiation, since a small contribution to the total radiation dose from neutrons involves gamma rays. Using binucleated cells with micronuclei (micronucleated cells) among in vitro monoenergetic-neutron-irradiated human lymphocytes as a measure of residual damage, we investigated the influence of the small gamma-ray contribution to the dose on suppressing residual damage.

Analysis of cell cycle in mouse bone marrow cells following acute in vivo exposure to 56Fe ions.

A pilot study was conducted to examine the magnitude of cell-cycle delay and apoptosis in bone marrow (BM) cells collected at 18, 42 and 66 hr from radiosensitive CBA/CaJ mice and radioresistant C57BL/6J mice following a whole-body in vivo exposure to 1 GeV/amu (56)Fe ions or (137)Cs gamma rays. At each sacrifice, BM cells were collected from three mice of each strain per dose of (56)Fe ions (0, 10 and 100 cGy) and two mice of each strain per dose of (137)Cs gamma rays (0, 100 and 300 cGy). A significant G1-arrest (ANOVA, p < 0.

Radiation leukemogenesis: a proteomic approach.

Objective: The objectives of this study were to identify protein biomarkers of radiation-induced acute myeloid leukemia (rAML) in CBA/CaJ mice, and to examine the similarities or differences in the patterns of protein-expression profiles among AMLs induced by low linear energy transfer (LET) radiation (e.g., gamma- or x-rays), and high LET radiation (i.

Activation of NF-kappaB in bone marrow cells of BALB/cJ mice following exposure in vivo to low doses of (137)Cs gamma-rays.

We measured levels of NF-kappaB activation in bone marrow (BM) cells collected at 1 and 4 h from male BALB/cJ mice (10-12 weeks old) given a whole body dose of 0, 0.05, 0.1 and 1 Gy of (137)Cs gamma-rays (at the dose rate of 0.