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      Reproductive hazards of space travel in women and men

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      Nature Reviews Endocrinology
      Springer Science and Business Media LLC

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          Abstract

          <p class="first" id="P3">Extended travel in deep space poses potential hazards to the reproductive function of female and male astronauts. These hazards include exposure to cosmic radiation, microgravity, increased gravity, psychological and physical stress, and circadian rhythm disruptions. This Review focuses on the effects of microgravity, hypergravity and cosmic radiation. Cosmic radiation contains protons and helium nuclei, as well as high charge and energy (HZE) particles. Studies performed on Earth in which rodents were exposed to experimentally generated HZE particles have demonstrated high sensitivity of ovarian follicles and spermatogenic cells to HZE particles. Exposure to microgravity during space flight and to simulated microgravity on Earth disrupts spermatogenesis and testicular testosterone synthesis in rodents, whereas the male reproductive system seems to adapt to exposure to moderate hypergravity. A few studies have investigated the effects of microgravity on female reproduction, and findings of disrupted oestrous cycling and in vitro follicle development are cause for concern. Many remaining data gaps need to be addressed, including the effects of microgravity, hypergravity and space radiation on the male and female reproductive tracts, hypothalamic–pituitary regulation of reproduction and prenatal development of the reproductive system, as well as the combined effects of the multiple reproductive hazards encountered in space. </p>

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          Research in microgravity is indispensable to disclose the impact of gravity on biological processes and organisms. However, research in the near-Earth orbit is severely constrained by the limited number of flight opportunities. Ground-based simulators of microgravity are valuable tools for preparing spaceflight experiments, but they also facilitate stand-alone studies and thus provide additional and cost-efficient platforms for gravitational research. The various microgravity simulators that are frequently used by gravitational biologists are based on different physical principles. This comparative study gives an overview of the most frequently used microgravity simulators and demonstrates their individual capacities and limitations. The range of applicability of the various ground-based microgravity simulators for biological specimens was carefully evaluated by using organisms that have been studied extensively under the conditions of real microgravity in space. In addition, current heterogeneous terminology is discussed critically, and recommendations are given for appropriate selection of adequate simulators and consistent use of nomenclature.
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            Cancer risk from exposure to galactic cosmic rays: implications for space exploration by human beings.

            Space programmes are shifting toward planetary exploration, and in particular towards missions by human beings to the moon and Mars. However, exposure to space radiation is an important barrier to exploration of the solar system by human beings because of the biological effects of high-energy heavy ions. These ions have a high charge and energy, are the main contributors to radiation risk in deep space, and their biological effects are understood poorly. Predictions of the nature and magnitude of risks posed by exposure to radiation in space are subject to many uncertainties. In recent years, worldwide efforts have focussed on an increased understanding of the oncogenic potential of galactic cosmic rays. A review of the new results in this specialty will be presented here.
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              Metabolic oxidation/reduction reactions and cellular responses to ionizing radiation: a unifying concept in stress response biology.

              Exposure of eukaryotic cells to ionizing radiation (IR) results in the immediate formation of free radicals that last a matter of milliseconds. It has been assumed that the subsequent alterations in multiple intracellular processes following irradiation is due to the initial oxidative damage caused by these free radicals. However, it is becoming increasingly clear that intracellular metabolic oxidation/reduction (redox) reactions can be affected by this initial IR-induced free radical insult and may remain perturbed for minutes, hours, or days. It would seem logical that these cellular redox reactions might contribute to the activation of protective or damaging processes that could impact upon the damaging effects of IR. These processes include redox sensitive signaling pathways, transcription factor activation, gene expression, and metabolic activities that govern the formation of intracellular oxidants and reductants. The physiological manifestations of these radiation-induced alterations in redox sensitive processes have been suggested to contribute to adaptive responses, bystander effects, cell cycle perturbations, cytotoxicity, heat-induced radiosensitization, genomic instability, inflammation, and fibrosis. While a great deal is known about the molecular changes associated with the initial production of free radicals at the time of irradiation, the contribution of perturbations in redox sensitive metabolic processes to biological outcomes following exposure to IR is only recently becoming established. This review will focus on evidence supporting the concept that perturbations in intracellular metabolic oxidation/reduction reactions contribute to the biological effects of radiation exposure as well as new concepts emerging from the field of free radical biology that may be relevant to future studies in radiobiology.
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                Author and article information

                Journal
                Nature Reviews Endocrinology
                Nat Rev Endocrinol
                Springer Science and Business Media LLC
                1759-5029
                1759-5037
                October 14 2019
                Article
                10.1038/s41574-019-0267-6
                7371565
                31611649
                fad71953-55ff-4879-8293-be30f03768b4
                © 2019

                http://www.springer.com/tdm

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