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Note: Students must purchase through Perusall to access the book in Perusall. Students can purchase online using a credit card, or your university's bookstore can order access codes from Perusall for students to purchase at the bookstore. Learn more. The subject matter contained in the current volume is viewed through the eyes of the radiation therapist.

Although the presentations have strong clinical overtones, an effort has been made, wherever possible, also to address the radiobiological bases of radiation sensitivity of organs. The book contains seven chapters and begins with a study on radiation damage to the kidney. While the lack of a solution to these concerns may seem surprising, the existence of the HZE particle component has been known only since , and biological research using heavy ions has been restricted to a very small number of centers in the world with suitable accelerators.

Furthermore, the critical experiments have proven difficult to carry out. The effects of HZE particles on the CNS include 1 cellular effects, including biochemical changes; 2 functional changes; and 3 late effects, especially DNA repair deficiencies. Cellular Effects High doses of low-LET radiation cause cellular changes and degeneration in neuronal tissues. Heavy ions are more effective in causing cellular damage, and the effects appear earlier than those appearing after exposure to low-LET radiation. In studies of the forebrain of rabbits, damage could be detected after exposure to 0.

For example, what is the effect of various radiation fluences on the centers in the floor of the fourth ventricle, the site of a number of centers including the cardiac and respiratory centers, in which there are closely packed neuron cell bodies? If traversal of neurons by the various HZE particles in the GCR does in fact result in early- or late-occurring damage, the fourth ventricle is an area of the brain that could be at risk there are also others.

This example indicates how little we know about the potential effects of radiation on the CNS. Without such information it is impossible to assess the potential risk of clinically important damage to the CNS that might result from crew members' exposure to radiation during long-duration missions in deep space.

Doses in the range of 0. Taste aversion has long been used as a test of behavioral and other changes induced by irradiation, and studies indicate that iron ions are more effective than lower-LET radiation in altering this particular type of behavior. Late Effects, Especially Repair Deficiencies Because many of the experiments concerning heavy ions have been associated with end points relevant to radiotherapy, questions about the effects on nonrenewing cell systems, especially the CNS, have remained unanswered.

Differentiated cells such as those in the CNS or the liver can incur relatively large doses of radiation of different qualities and still retain their function. What is not known is whether untoward effects may appear later. The integrity of the transcribing regions of the genome must be reserved to ensure the fidelity of the RNA transcripts and also of the proteins, translated from RNA, that are necessary for the correct functioning of cells. Changes with age in the retinal DNA of rabbits after irradiation have been studied by Lett and his coworkers.

The age at which secondary changes in the DNA of the photoreceptor occurred decreased with an increase in the LET of the radiation.


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The secondary changes in the DNA occurred earlier and were more marked with iron ions than with other heavy charged particles or with photons. Significant effects were noted after exposure at 2 to 3 Gy of iron ion radiation. If it is assumed that the photoreceptors are a reasonable surrogate for neurons in the CNS, then the above results suggest that it is necessary to obtain adequate dose-response data using the most sensitive techniques for detecting DNA damage.

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Furthermore, it is mandatory to determine whether or not breakdown of DNA, which is an indication of impending cell death, occurs many years after exposure to radiation. As yet, there are no complete data for RBE-LET relationships for the relevant end points for assessing the risk of radiation-induced damage. Cataracts are considered a hazard of exposure to radiation, and limits for exposure are set for terrestrial workers who deal with radiation sources. The limits are based on estimates from studies of humans exposed to low-LET radiation.

There is considered to be a threshold dose below which lenticular opacities of clinical importance do not occur. For this reason, cataract induction is considered a deterministic effect. However, the threshold is more a matter of the level of detection capable of detecting the beginning of cataractogenesis, and the most likely mechanism is consistent with a stochastic effect.

Assessing the risk of cataractogenesis from irradiation in space, in particular in deep-space missions, requires a knowledge of the associated RBE values of the various types of radiation. There are no data for induction of cataracts in humans exposed to HZE particles, and only sparse data for induction by protons. Thus, reliance on data from animal experiments is necessary. The sensitivity of the lens of different species varies by more than an order of magnitude, decreasing with increasing size.

In humans, a threshold dose for low-LET radiation of about 2. For the atomic bomb survivors, a somewhat lower threshold dose, 1. Data from patients receiving radiotherapy or irradiation prior to bone marrow transplantation suggest a significant decrease, perhaps on the order of fivefold, in cataractogenic effects compared with the number induced by single high-dose-rate exposures.

On the basis of experiments with rats, 69 no such sparing would be predicted for the effects of exposure to very high LET radiation. Evidence from studies on monkeys indicates that the cataractogenic effect of protons will not be very different from that of gamma rays. The estimates of the risk of cataract induction from exposure to heavy ions are somewhat disparate, 71 , 72 and until more definitive estimates are in hand, relatively high RBE values should be used in calculating the equivalent doses for estimating risk.

The great majority of data on the assessment of genetic or heritable effects in human populations following exposure to radiation has come from studies of the atomic bomb survivors. The following end points have been assessed: untoward pregnancy outcomes major congenital malformation, stillbirth, neonatal death ; sex of child; tumors with onset prior to the age of 20; death of liveborn infants through an average age of There were no significant increases in any of these indicators from a combined parental gonadal equivalent dose of 0.

A recent study by Kodaira et al.

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A similar result was reported by Satoh et al. UNSCEAR 76 made estimates of the unirradiated background incidence of mutational effects per generation for the end points studied on the acutely exposed Japanese population. Allowing for chronic exposure, a gonadal dose reduction factor was applied to give a minimal estimated doubling dose of 4 Sv for genetic effects. Hence the actual increase above background in heritable effects per locus, depending on the particular locus, and the risk of heritable effects to individuals engaged in extended space travel will be low.

In addition, because the number of individuals who might be exposed to ionizing radiation during long-range spaceflight will represent a very small fraction of the population, any genetic risk to the human gene pool would be negligible. The rapid increase in knowledge of the mechanisms of tumor induction and heritable effects has led to a clear appreciation of the potential for a genetic predisposition to the induction of cancer by exogenous agents and endogenous processes and to induction of heritable changes.

Such a predisposition might be specific for a single agent such as ionizing radiation e. Given that within the normal human population a range of risk exists for induction of cancer, it is difficult at this time to assign a value for increased risk owing to a single genetic susceptibility. In general, most of the genetic susceptibility or sensitivity factors that are common in the population tend to increase relative risk by small amounts. Those conferring high relative risk are present at a low frequency.

The latter is particularly true for susceptibility for which background frequencies of cancer are high. It has become increasingly apparent that the sensitivity of cells to radiation is controlled in part by the relationship of DNA repair kinetics to cell cycle progression. The quintessential example is the gene p53, which is involved in cell cycle control at the G 1 checkpoint, the time point in the cell cycle at which DNA synthesis begins, and in the repair of DNA damage either directly or indirectly.

The question of interest then is, What kinds of genotypes might elicit increases in sensitivity to radiation? For example, it is apparent that control of the cell cycle is a very complex process involving in part the interactions of cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors. Alterations in any of these components could lead to abrogation in the cell cycle control, which would lead to abnormal responses to DNA damage and an increased sensitivity to genetic alteration. It remains of considerable importance to understand the mechanisms of genetic instability arising from abrogation of control at checkpoints in the cell cycle, and to determine the effects these mechanisms can have on radiosensitivity.

Work in this area by the wider community of cancer investigators would lead to understanding of the role of genetic instability in cancer predisposition, and to development of assays for detecting individuals at increased risk. While there will be a range of genotypes among individuals selected for long-range spaceflight, there is a very low probability that there will be highly sensitive individuals in the group.


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  • Very specific genotypes, such as those giving rise to ataxia telangiectasia and Li-Fraumeni syndrome, are obvious phenotypically, and such individuals would not constitute part of the selection pool. More subtle individual differences in sensitivity to ionizing radiation would not be detectable phenotypically. It could be argued that a radiosensitivity assay G 2 sensitivity such as that described by Scott et al. However, such an assay is not, at present, directly predictive of an increased sensitivity to an adverse health outcome.

    Hence, it is appreciated by cancer investigators that a more complete assessment of the G 2 sensitivity assay needs to be conducted in order to establish its range of sensitivity and possible predictive capability for cancer or heritable effects.

    Description

    The repair mechanisms utilized by the human body after exposure to radiation are an important part of any discussion of radiation effects, and the repair of damage to DNA is of obvious interest when considering late effects such as cancer. It has been known for a number of years that sophisticated and complex cellular processes exist for repairing all types of DNA damage: single-strand breaks, double-strand breaks, and a wide variety of types of base damage, all of which can result from exposure to radiation. In the past 5 years, the repair processes for handling DNA damage have been largely characterized at the molecular level, and their complexity has been established.

    It is interesting to note that several of the repair processes are modifications of the functions of other cellular housekeeping proteins, such as transcription complexes or cell cycle control genes. The very specific incisions required for removal of DNA damage are produced by enzymes of this complex. Reviews by Wood et al. While the actual process of excising damaged nucleotides by NER is quite well worked out, the cellular control and damage recognition processes are still the subject of extensive research efforts.

    More recently, an understanding of repair of DNA damage induced by ionizing radiation has emerged. Two recent reviews, one on the repair of oxidative damage 86 and a second on double-strand break repair, 87 describe the current level of knowledge. The enzymology of repair of some damaged bases and sugars has been quite thoroughly described in bacterial systems and to a lesser extent in S. In broad terms, the process of base and sugar damage repair involves damage recognition, base excision of purine or pyrimidines, site incision, and fragment release.

    Clearly, variations in efficiency among cell types or species, or within a population, can occur at any one of these steps, each of which is under genetic control. At this time, however, no human syndrome has been identified that results in a sensitivity to ionizing radiation attributable to a deficiency in the repair of oxidative damage. The understanding of the mechanism of repair of DNA double-strand breaks has taken several significant steps forward recently.

    Studies have demonstrated that there is a close association between the repair of site-specific double-strand breaks introduced during V D J recombination and those generated by DNA-damaging agents. It has been shown that several radiosensitive mammalian mutants are defective in Ku80, that cells from severe combined immunodeficient scid mice have a DNA repair defect, and that additional radiosensitive cell lines have a deficiency in DNA-PK cs.

    It has been suggested that there could be a link between double-strand break repair machinery and transcription, as has been described for NER. To date, no human syndromes that are characterized by defects in DNA-PK have been identified, although the DNA-PK cs gene maps to the same human chromosome region as the one for the human gene that complements scid. A good deal has been learned about repair mechanisms by studying the human syndrome ataxia telangiectasia AT , which is characterized by a sensitivity to cell killing and mutation induction in cells in vitro as a result of exposure to low-LET x rays, and, in some cases, by a loss of x-ray-induced inhibition of initiation of DNA synthesis.

    It was presumed by investigators that these phenotypes were the consequence of a DNA repair defect, and that different steps or components were controlled by genes in the four different complementation groups, all of which map to a single chromosome region. However, the recent cloning of the AT mutated gene ATM 97 and additional characterization of homologous genes in yeast 98 , 99 have shown that the defect in AT cells is not the result of a repair defect but results from an altered cell cycle control, and perhaps an inability to activate damage-inducible DNA repair.

    The radiosensitivity and cancer susceptibility of ATM homozygotes are well established and very clear-cut. On the other hand, whether or not there is increased sensitivity in ATM heterozygotes is less clear. It has been reported that there is an increased breast cancer risk for ATM heterozygotes, although this remains equivocal.

    Recently, Scott et al. Thus, heterozygosity for DNA repair genes, where the phenotype is not immediately apparent, could be a marker for susceptibility to cancer, particularly following exposure to ionizing radiation. It is expected that screening for ATM heterozygosity will soon be possible based on recent reports of the genomic organization and gene sequence. A growing understanding of the various mechanisms of repair of ionizing radiation-induced DNA damage, and of the effects of mutations in genes involved in the repair itself or in its control, is likely to greatly aid in predicting the risk of adverse biological effects arising from exposure to radiation, and eventually in identifying individuals at increased risk.

    Over many years, NASA maintained only a very small radiation health program because of the responsibility, mandated to the Department of Energy DOE and its predecessors, for radiation studies. Recently, the funding for NASA radiation research has increased. However, although the percentage increase in funding has been large, the budget in years past was small. Moreover, DOE has significantly reduced its funding for radiation studies in the last few years. Major radiation and animal facilities have been closed, including the high-LET radiation sources for experimental studies at Oak Ridge and Argonne national laboratories.

    DOE funding of the important facility at Columbia University has been terminated, and the future of the radiation facilities at the Armed Forces Radiobiology Research Institute is now threatened. BEVALAC, the only facility in the United States that was producing beams of heavy ion spectra of energy and LET suitable for cellular and animal studies, as well as for investigations of fragmentation and aspects important for dosimetry, was closed by DOE in As noted by several previous advisory groups see, for example, Appendix D , this closure has had very serious consequences for efforts to estimate risks from exposure to radiation in deep space.

    Two accelerators, one in Germany and one in Japan, have been developed for heavy ion radiotherapy see Appendix C and could be of use in the NASA program. There is no question that international collaboration involving accelerators with guarantees of appropriate particles and beam time , personnel to operate and use the facilities , and the necessary financial commitments would be of help in carrying out the priority experiments outlined in Chapter 4.

    The present U. At this rate of utilization, it would take more than 20 years to obtain the physical and biological data needed to make rational decisions about the shielding needed to protect space crews from the biological effects of radiation in space see Chapter 4. Collaborative efforts cannot involve transfer of animals among international sites because of strict national quarantine restrictions aimed at reducing the spread of potentially hazardous microorganisms and viruses.

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    Moreover, the travel of animals over a number of time zones would force a resetting of their biological clocks, during which time they would be physiologically and psychologically altered and not useful for controlled experiments. Hence, a requirement for international efforts is the establishment of identical animal colonies at international sites so as to eliminate scientific and legalistic impediments and any effects of biological variability in experimental results.

    All animal colonies, for example, would have to conform to international accreditation standards, and animal experiments would have to be approved by local institutional review boards and by the board of a collaborating investigator's institution. Lemaignen, L. Document No. DDT Simonsen, L. Temporal analysis of the October proton flare using computerized anatomical models. Curtis, S. Risk cross sections and their application to risk estimation in the galactic cosmic-ray environment. Badhwar, G. Galactic cosmic radiation model and its applications. Guidance on Radiation Received in Space Activities.

    Conklin, J. Military Radiobiology. Academic Press, Orlando, Fla. See also Conklin and Walker, eds. Radakovich, M. The effect of total body irradiation on wound closure. See also Raventos, A. Wound healing and mortality after total body exposure to ionizing radiation. Raventos, , Wound healing and mortality after total body exposure to ionizing radiation. See also Lawrence, W. Roentgen rays and wound healing: experimental study. Surgery — Meistrich, M.

    Radiation sensitivity of the human testes. Hahn, E. Recovery from aspermia induced by low-dose radiation in seminoma patients. Cancer — Lushbaugh, C. Effects of gonadal irradiation in clinical radiation therapy: A review. Ash, P. The influence of radiation on fertility in man. Damewood, M. Prospects for fertility after chemotherapy or radiation for neoplastic disease.

    General Assembly Official Records: 17th Session. Supplement No. United Nations, New York. Annex F: Influence of dose and dose rate on stochastic effects of radiation. Risk Estimates for Radiation Protection. Yochmowitz, M. Seventeen-year mortality experience of proton radiation in Macaca mulatta. Clapp, N.

    Relative effects of whole-body sublethal doses of MeV protons and kVp x rays on disease incidence in RF mice. Burns, F. The dose-response curve for tumor induction with single and split doses of 10 MeV protons. Hall, E. The relative biological effectiveness of MeV protons. Raju, M. A heavy particle comparative study. Part II: Cell survival versus depth. Todorov, S. Dose response relationship for chromosomal aberrations induced by x rays or 50 MeV protons in human peripheral lymphocytes. Edwards, A. Chromosome aberrations in human lymphocytes by 8. Alpen, E. Fluence based relative biological effectiveness for charged particle carcinogenesis in mouse Harderian gland.

    Blakely, E. Heavy ion radiobiology: Cellular studies. Kronenberg, A. NASA space radiation health program: Ground based radiobiology research program. Kadhim, M. BMC Cancer 9 Zhou, D. A high dose of ionizing radiation induces tissue-specific activation of nuclear factor-kappaB in vivo. Das, U. Role of ferulic acid in the amelioration of ionizing radiation induced inflammation: a murine model. PLoS One 9 :e Dent, P. Stress and radiation-induced activation of multiple intracellular signaling pathways. MAPK pathways in radiation responses.

    Oncogene 22 — Bak, J. Oxid Med Cell Longev Kang, Y. Regulation of intracellular cyclooxygenase levels by gene transcription and protein degradation. Prog Lipid Res 46 — Immenschuh, S. Heme oxygenase-1 and iron in liver inflammation: a complex alliance. Curr Drug Targets 11 — Farombi, E. Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. J Biochem Mol Biol 39 — PubMed Google Scholar. Benson, R.

    Radiation induced liver disease: A clinical update. J Egypt Natl Canc Inst 28 :7—11 Lin, C. Cell Commun Signal 11 :8 Motino, O. Cyclooxygenase-2 expression in hepatocytes attenuates non-alcoholic steatohepatitis and liver fibrosis in mice. Biochim Biophys Acta — Tang, S. Mol Med Rep 15 : — Fabregat, I. TGF-beta signalling and liver disease. FEBS J — Protective effects of Korean red ginseng against radiation-induced apoptosis in human HaCaT keratinocytes. J Radiat Res 55 — El-Tanbouly, D.

    Toxicol Appl Pharmacol —