Space travel has advanced significantly over the last six decades with astronauts spending up to 6 months at the International Space Station. Nonetheless, the living environment while in outer space is extremely challenging to astronauts. In particular, exposure to space radiation represents a serious potential long-term threat to the health of astronauts because the amount of radiation exposure accumulates during their time in space. Therefore, health risks associated with exposure to space radiation are an important topic in space travel, and characterizing space radiation in detail is essential for improving the safety of space missions. In the first part of this review, we provide an overview of the space radiation environment and briefly present current and future endeavors that monitor different space radiation environments. We then present research evaluating adverse biological effects caused by exposure to various space radiation environments and how these can be reduced. We especially consider the deleterious effects on cellular DNA and how cells activate DNA repair mechanisms. The latest technologies being developed, e.g., a fluorescent ubiquitination-based cell cycle indicator, to measure real-time cell cycle progression and DNA damage caused by exposure to ultraviolet radiation are presented. Progress in examining the combined effects of microgravity and radiation to animals and plants are summarized, and our current understanding of the relationship between psychological stress and radiation is presented. Finally, we provide details about protective agents and the study of organisms that are highly resistant to radiation and how their biological mechanisms may aid developing novel technologies that alleviate biological damage caused by radiation. Future research that furthers our understanding of the effects of space radiation on human health will facilitate risk-mitigating strategies to enable long-term space and planetary exploration.

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and Aomori-2, were isolated from FIV-seropositive domestic cats in Japan, and their proviral DNAs were amplified by PCR. The nucleotide sequences of their env and gag genes were determined and compared with those of previously described isolates: U.S. and European isolates and one Japanese isolate, TM2. Phylogenetic analyses of complete env gene sequences demonstrate that worldwide isolates are classified into three subtypes: Japanese TM2, Japanese Shizuoka, and non-Japanese subtypes (U.S. and European isolates), with 20% amino acid distances from each other. This pattern indicates that an evolutionary radiation of these three subtypes of FIV occurred at approximately the same time. The sequence data of gag genes also confirmed these results. Furthermore, the Sendai-1 isolate was identified as an imported FIV isolate.

Ikaros (now known as Znfn1a1), a Krüppel-type zinc-finger transcription factor that plays a critical role in both lineage commitment and differentiation of lymphoid cells, has recently been shown to function as a tumor suppressor gene. We have previously reported a high frequency of LOH (approximately 50%) at the Znfn1a1 locus in radiation-induced T-cell lymphoma in susceptible B6C3F1 mice. The aim of the present study was to delineate the types of Znfn1a1 inactivation, with special reference to the LOH status, and to determine the relative contribution of each type of Znfn1a1 inactivation in radiation-induced T-cell lymphomas in B6C3F1 mice. We demonstrated that Znfn1a1 was frequently altered (in approximately 50% of T-cell lymphomas), and that its inactivation was caused by a variety of mechanisms, which came under one of the following four categories: (1) null expression (14%); (2) expression of unusual dominant-negative isoforms (11%); (3) amino acid substitutions in the N-terminal zinc-finger domain for DNA binding caused by point mutations (22%); (4) lack of the Znfn1a1 isoform 1 due to the creation of a stop codon by insertion of a dinucleotide in exon 3 (3%). The null expression, amino acid substitutions, and dinucleotide insertion inactivation types were well correlated with LOH at the Znfn1a1 allele (86%) and were consistent with Knudson's two-hit theory. On the other hand, T-cell lymphomas expressing dominant-negative Znfn1a1 isoforms retained both alleles. These results indicate that Znfn1a1 inactivation takes place by a variety of mechanisms in radiation-induced murine T-cell lymphomas and is frequently associated with LOH, this association depending on the type of inactivation.

Children are especially sensitive to ionizing radiation and chemical carcinogens, and limiting their cancer risk is of great public concern. Calorie restriction (CR) is a potent intervention for suppressing cancer. However, CR is generally not appropriate for children. This study, therefore, examined to see if adult-onset CR influences the lifetime cancer risk in mice after early-life exposure to ionizing radiation. Infant male mice (1-week-old) were exposed to 3.8 Gy X-rays, fed a control 95 kcal/week or CR 65 kcal/week diet from 7 weeks of age (adult stage), and their lifespan and tumor development were assessed. Irrespective of CR, X-rays shortened lifespan by 38%, and irrespective of irradiation CR extended lifespan by 20%. Thymic lymphoma (TL) and early-occurring non-TL were induced by radiation. The liver and Harderian gland were more susceptible to radiation-induced tumors than the lungs and non-thymic lymphoid tissues (late occurring). CR reduced the risk of hepatocellular carcinoma, late-occurring non-TL, lung tumor, Harderian tumor, and hemangioma but had less impact on TL and early-occurring non-TL. Most notably, the effects of X-rays on induction of lung tumors, late-occurring non-TL and hemangioma were essentially canceled by CR. The ability of CR to prevent late-occurring tumors was the same for non-irradiated and irradiated mice, indicating that the mechanism by which CR influences cancer is independent of irradiation. Our results indicate that adult-onset CR significantly inhibits late-occurring tumors in a tissue-dependent manner regardless of infant radiation exposure.