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1.
J Radiat Res ; 57(4): 325-35, 2016 Jul.
Article in English | MEDLINE | ID: mdl-27242342

ABSTRACT

Both psychological stress (PS) and ionizing radiation (IR) cause varied detrimental effects on humans. There has been no direct evidence so far showing PS alone could cause cancer; however, long-lasting PS may affect our overall health and ability to cope with cancer. Due to their living conditions and occupations, some people may encounter concurrent exposure to both PS and IR to a high extent. In addition to possible health effects resulting directly from exposure to IR on these people, fear of IR exposure is also a cause of PS. The question of whether PS would influence susceptibility to IR, radiocarcinogenesis in particular, is of great concern by both the academic world and the public. Recently, investigations using animal PS models demonstrated that PS could modulate susceptibility to IR, causing increased susceptibility to radiocarcinogenesis in Trp53-heterozygous mice, hematological toxicity in peripheral blood and elevated chromosome aberration (dicentrics) frequency in splenocytes of Trp53-wild-type mice. To actively reduce health risk from exposure to IR, further studies are needed to cumulate more evidence and provide insights into the mechanisms underlying the alterations in susceptibility due to PS modulation. This mini-review gives a general overview of the significance of PS effects on humans and experimental animals, with a special focus on summarizing the latest weight-of-evidence approaches to radiobiological studies on PS-induced alterations in susceptibility in experimental animal models. The susceptibility being investigated is mainly in the context of the impact of the modulatory effect of PS on radiocarcinogenesis; we seek to improve understanding of the combined effects of exposure to both PS and IR in order to facilitate, via active intervention, strategies for radiation risk reduction.


Subject(s)
Health , Radiation, Ionizing , Stress, Psychological/complications , Animals , Disease Models, Animal , Humans
2.
J Neurosci Res ; 92(7): 915-26, 2014 Jul.
Article in English | MEDLINE | ID: mdl-24936619

ABSTRACT

The cause and risk factors of Alzheimer's disease (AD) are largely unknown. Studies on possible radiation-induced AD-like pathogenesis and behavioral consequences are important because humans are exposed to ionizing radiation (IR) from various sources. It was reported that total-body irradiations (TBI) at 10 cGy of low linear energy transfer (LET) X-rays to mice triggered acute transcriptional alterations in genes associated with cognitive dysfunctions. However, it was unknown whether low doses of IR could induce AD-like changes late after exposure. We reported previously that 10 cGy X-rays induced early transcriptional response of several AD-related genes in hippocampi without late AD-like pathogenesis and memory impairment in mice. Here, further studies on two low doses (5 or 10 cGy) of high LET carbonion irradiations are reported. On expression of 84 AD-related genes in hippocampi, at 4 hr after TBI, 5 cGy induced a significant upregulation of three genes (Abca1, Casp3, and Chat) and 10 cGy led to a marked upregulation of one gene (Chat) and a downregulation of three genes (Apoe, Ctsd, and Il1α), and, at 1 year after TBI, one gene (Il1α) was significantly downregulated in 10 cGy-irradiated animals. Changes in spatial learning ability and memory and induction of AD-like pathogenesis were not detected by in vivo brain imaging for amyloid-ß peptide accumulation and by immunohistochemical staining of amyloid precursor protein, amyloid-ß protein, tau, and phosphorylated tau protein. These findings indicate that low doses of carbon-ion irradiations did not cause behavioral impairment or AD-like pathological change in mice.


Subject(s)
Alzheimer Disease/etiology , Carbon/adverse effects , Gene Expression Regulation/radiation effects , Memory Disorders/etiology , Whole-Body Irradiation/adverse effects , Alzheimer Disease/diagnostic imaging , Alzheimer Disease/pathology , Amyloid beta-Peptides/metabolism , Animals , Disease Models, Animal , Dose-Response Relationship, Radiation , Female , Hippocampus/diagnostic imaging , Hippocampus/metabolism , Hippocampus/radiation effects , Linear Energy Transfer , Magnetic Resonance Imaging , Maze Learning/radiation effects , Memory Disorders/diagnostic imaging , Memory Disorders/pathology , Mice , Mice, Inbred C57BL , Positron-Emission Tomography , Time Factors , tau Proteins/metabolism
3.
J Radiat Res ; 55(1): 84-96, 2014 Jan 01.
Article in English | MEDLINE | ID: mdl-23908553

ABSTRACT

The cause and progression of Alzheimer's disease (AD) are poorly understood. Possible cognitive and behavioral consequences induced by low-dose radiation are important because humans are exposed to ionizing radiation from various sources. Early transcriptional response in murine brain to low-dose X-rays (100 mGy) has been reported, suggesting alterations of molecular networks and pathways associated with cognitive functions, advanced aging and AD. To investigate acute and late transcriptional, pathological and cognitive consequences of low-dose radiation, we applied an acute dose of 100-mGy total body irradiation (TBI) with X-rays to C57BL/6J Jms mice. We collected hippocampi and analyzed expression of 84 AD-related genes. Mouse learning ability and memory were assessed with the Morris water maze test. We performed in vivo PET scans with (11)C-PIB, a radiolabeled ligand for amyloid imaging, to detect fibrillary amyloid beta peptide (Aß) accumulation, and examined characteristic AD pathologies with immunohistochemical staining of amyloid precursor protein (APP), Aß, tau and phosphorylated tau (p-tau). mRNA studies showed significant downregulation of only two of 84 AD-related genes, Apbb1 and Lrp1, at 4 h after irradiation, and of only one gene, Il1α, at 1 year after irradiation. Spatial learning ability and memory were not significantly affected at 1 or 2 years after irradiation. No induction of amyloid fibrillogenesis or changes in APP, Aß, tau, or p-tau expression was detected at 4 months or 2 years after irradiation. TBI induced early or late transcriptional alteration in only a few AD-related genes but did not significantly affect spatial learning, memory or AD-like pathological change in mice.


Subject(s)
Alzheimer Disease/etiology , Alzheimer Disease/physiopathology , Memory Disorders/etiology , Memory Disorders/physiopathology , Radiation Injuries/etiology , Radiation Injuries/physiopathology , Whole-Body Irradiation/adverse effects , Animals , Dose-Response Relationship, Radiation , Female , Longitudinal Studies , Mice , Mice, Inbred C57BL , Radiation Dosage , Spatial Learning/radiation effects , X-Rays
4.
J Radiat Res ; 53(6): 815-22, 2012 Nov 01.
Article in English | MEDLINE | ID: mdl-22872779

ABSTRACT

Alzheimer's disease (AD) is a human neurodegenerative disease, and its global prevalence is predicted to increase dramatically in the following decades. There is mounting evidence describing the effects of ionizing radiation (IR) on the brain, suggesting that exposure to IR might ultimately favor the development of AD. Therefore better understanding the possible connections between exposure to IR and AD pathogenesis is of utmost importance. In this review, recent developments in the research on the biological and cognitive effects of IR in the brain will be explored. Because AD is largely an age-related pathology, the effects of IR on ageing will be investigated.


Subject(s)
Aging/radiation effects , Alzheimer Disease/epidemiology , Alzheimer Disease/physiopathology , Brain/physiopathology , Brain/radiation effects , Radiation Injuries/epidemiology , Radiation Injuries/physiopathology , Alzheimer Disease/etiology , Environmental Exposure/adverse effects , Environmental Exposure/statistics & numerical data , Humans , Prevalence , Radiation Injuries/etiology , Radiation, Ionizing , Risk Assessment
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