Adaptive Response of Low Linear Energy Transfer <scp>X</scp>‐rays for Protection Against High Linear Energy Transfer Accelerated Heavy Ion‐Induced Teratogenesis

Wang, Bing; Ninomiya, Yasuharu; Tanaka, Kaoru; Maruyama, Kouichi; Varès, Guillaume; Eguchi-Kasai, Kiyomi; Nenoi, Mitsuru

doi:10.1002/bdrb.21027

Cited by 8 publications

(17 citation statements)

References 32 publications

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“…Rithidech and Scott [ 77 ] proposed that the protective mechanisms could be triggered in cells by a gamma-component that is produced within a body upon exposure to neutrons [ 78 ]. Additionally, it has been shown that low doses of low LET radiation may render resistance to genotoxicity and teratogenesis induced by high doses of HZE particles [ 75 , 79 ]. Intriguingly, priming normal human cells with low doses of energetic protons resulted in lower chromosomal damage induced by subsequent exposure to iron ions [ 80 ].…”

Section: Radiation Dna Damage and Mechanisms Of Repairmentioning

confidence: 99%

Vive la radiorésistance!: converging research in radiobiology and biogerontology to enhance human radioresistance for deep space exploration and colonization

et al. 2018

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While many efforts have been made to pave the way toward human space colonization, little consideration has been given to the methods of protecting spacefarers against harsh cosmic and local radioactive environments and the high costs associated with protection from the deleterious physiological effects of exposure to high-Linear energy transfer (high-LET) radiation. Herein, we lay the foundations of a roadmap toward enhancing human radioresistance for the purposes of deep space colonization and exploration. We outline future research directions toward the goal of enhancing human radioresistance, including upregulation of endogenous repair and radioprotective mechanisms, possible leeways into gene therapy in order to enhance radioresistance via the translation of exogenous and engineered DNA repair and radioprotective mechanisms, the substitution of organic molecules with fortified isoforms, and methods of slowing metabolic activity while preserving cognitive function. We conclude by presenting the known associations between radioresistance and longevity, and articulating the position that enhancing human radioresistance is likely to extend the healthspan of human spacefarers as well.

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Section: Radiation Dna Damage and Mechanisms Of Repairmentioning

confidence: 99%

Vive la radiorésistance!: converging research in radiobiology and biogerontology to enhance human radioresistance for deep space exploration and colonization

et al. 2018

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“…Prenatal LDIR exposure induces teratogenesis and mortality [55–61] (Table 5). In female CF1 and BALB/c strain mice, irradiation with X-rays (100 mGy) at 7 h post fertilization resulted in increased frequency of malformed fetuses and Dwarfism occurrence when examined 18 days later.…”

Section: Ldir and Ldrir-induced Bionegative Effects In Animal Modelsmentioning

confidence: 99%

“…A single 10 mGy CT scan or PET scan (7–22 mSv) of Trp53 +/− female mice significantly extended the overall lifespan of these mice relative to the controls [92]. Primary conditioning with low doses of radiation was also reported to significantly suppress incidences of teratogenesis induced by a follow-on high dose of radiation [60, 61, 93]. In genetically susceptible ApoE −/− mice with normal p53 function, γ-radiation exposures at doses as low as 25 mGy, given at either an early or late stage of the disease, protected against atherosclerosis in a manner distinctly non-linear with respect to dose [94].…”

Section: Ldir/ldrir–induced Biopositive Effects In Animalsmentioning

confidence: 99%

Low-dose or low-dose-rate ionizing radiation–induced bioeffects in animal models

Tang

Loke

Khoo

2016

Journal of Radiation Research

120

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Animal experimental studies indicate that acute or chronic low-dose ionizing radiation (LDIR) (≤100 mSv) or low-dose-rate ionizing radiation (LDRIR) (<6 mSv/h) exposures may be harmful. It induces genetic and epigenetic changes and is associated with a range of physiological disturbances that includes altered immune system, abnormal brain development with resultant cognitive impairment, cataractogenesis, abnormal embryonic development, circulatory diseases, weight gain, premature menopause in female animals, tumorigenesis and shortened lifespan. Paternal or prenatal LDIR/LDRIR exposure is associated with reduced fertility and number of live fetuses, and transgenerational genomic aberrations. On the other hand, in some experimental studies, LDIR/LDRIR exposure has also been reported to bring about beneficial effects such as reduction in tumorigenesis, prolonged lifespan and enhanced fertility. The differences in reported effects of LDIR/LDRIR exposure are dependent on animal genetic background (susceptibility), age (prenatal or postnatal days), sex, nature of radiation exposure (i.e. acute, fractionated or chronic radiation exposure), type of radiation, combination of radiation with other toxic agents (such as smoking, pesticides or other chemical toxins) or animal experimental designs. In this review paper, we aimed to update radiation researchers and radiologists on the current progress achieved in understanding the LDIR/LDRIR-induced bionegative and biopositive effects reported in the various animal models. The roles played by a variety of molecules that are implicated in LDIR/LDRIR-induced health effects will be elaborated. The review will help in future investigations of LDIR/LDRIR-induced health effects by providing clues for designing improved animal research models in order to clarify the current controversial/contradictory findings from existing studies.

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“…In addition, teratogenic effects induced in fetal mice could be attenuated by an adaptive response using an X-ray priming dose followed by exposure to monoenergetic C-ions, neon ions, silicon (LET values 15, 30, 55 keV/μm) but not when using iron ions (200 keV/μm) for the challenge dose [ 241 , 242 ]. This suggests possible specific radiation quality effects of the challenge radiation.…”

Section: Ionizing Radiation (Ir) Effects Involving Mitochondriamentioning

confidence: 99%

Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts

Averbeck

Rodriguez-Lafrasse

2021

IJMS

115

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Until recently, radiation effects have been considered to be mainly due to nuclear DNA damage and their management by repair mechanisms. However, molecular biology studies reveal that the outcomes of exposures to ionizing radiation (IR) highly depend on activation and regulation through other molecular components of organelles that determine cell survival and proliferation capacities. As typical epigenetic-regulated organelles and central power stations of cells, mitochondria play an important pivotal role in those responses. They direct cellular metabolism, energy supply and homeostasis as well as radiation-induced signaling, cell death, and immunological responses. This review is focused on how energy, dose and quality of IR affect mitochondria-dependent epigenetic and functional control at the cellular and tissue level. Low-dose radiation effects on mitochondria appear to be associated with epigenetic and non-targeted effects involved in genomic instability and adaptive responses, whereas high-dose radiation effects (>1 Gy) concern therapeutic effects of radiation and long-term outcomes involving mitochondria-mediated innate and adaptive immune responses. Both effects depend on radiation quality. For example, the increased efficacy of high linear energy transfer particle radiotherapy, e.g., C-ion radiotherapy, relies on the reduction of anastasis, enhanced mitochondria-mediated apoptosis and immunogenic (antitumor) responses.

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Adaptive Response of Low Linear Energy Transfer X‐rays for Protection Against High Linear Energy Transfer Accelerated Heavy Ion‐Induced Teratogenesis

Abstract: Successful AR induction appears to be a radiation quality event, depending on the LET value and/or the particle species of the challenge irradiations. These findings would provide a new insight into the study on radiation-induced AR in utero.

Cited by 8 publications

References 32 publications

Vive la radiorésistance!: converging research in radiobiology and biogerontology to enhance human radioresistance for deep space exploration and colonization

Vive la radiorésistance!: converging research in radiobiology and biogerontology to enhance human radioresistance for deep space exploration and colonization

Low-dose or low-dose-rate ionizing radiation–induced bioeffects in animal models

Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts

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