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The molecular theory of radiation biology

Author: K H Chadwick; H P Leenhouts
Publisher: Berlin ; New York : Springer-Verlag, 1981.
Series: Monographs on theoretical and applied genetics, v. 5.
Edition/Format:   Print book : EnglishView all editions and formats
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Genre/Form: Molekulare Strahlenbiologie
Additional Physical Format: Online version:
Chadwick, K.H. (Kenneth Helme).
Molecular theory of radiation biology.
Berlin ; New York : Springer-Verlag, 1981
(OCoLC)561028408
Document Type: Book
All Authors / Contributors: K H Chadwick; H P Leenhouts
ISBN: 0387102973 9780387102979 3540102973 9783540102977
OCLC Number: 6862725
Description: xvi, 377 pages : illustrations ; 25 cm.
Contents: 1. Quantitative Radiation Biology.- 1.1 Radiation in Society.- 1.2 Radiation Biology: the Interdisciplinary Discipline.- 1.3 The Importance of Cellular Biology.- 1.4 The Quantitative Analysis of Radiation Action: a Brief Historical Review.- 1.5 Desiderata for a Quantitative Theory of Radiation Biology.- 2. The DNA Molecule and Its Role in the Cell.- 2.1 Introduction.- 2.2 The Structure and Dimensions of the DNA Molecule.- 2.3 Base Sequences and the Genetic Code.- 2.4 DNA Replication.- 2.5 DNA in Chromosomes.- 2.6 The Diploid Cell, Mitosis and Meiosis.- 2.7 Radiation-Induced Damage to DNA.- 2.7.1 DNA Base Damage.- 2.7.2 DNA Single Strand Breaks.- 2.7.3 DNA Double Strand Breaks.- 3. The Molecular Model for Cell Survival Following Radiation.- 3.1 Historical Development.- 3.2 The Philosophical Framework of the Model.- 3.3 The Induction of DNA Double Strand Breaks by Radiation.- 3.3.1 The Induction of DNA Single Strand Breaks.- 3.3.2 The Induction of DNA Double Strand Breaks in One Radiation Event.- 3.3.3 The Induction of DNA Double Strand Breaks in Two Radiation Events.- 3.3.4 The Total Induction of DNA Double Strand Breaks.- 3.3.5 The Induction of DNA Double Strand Breaks with Repair.- 3.3.6 The Influence of Base Damage on the Production of Double Strand Breaks.- 3.4 The Relationship Between Cell Survival and DNA Double Strand Breaks.- 3.5 The Cell Survival Curve.- 3.5.1 Cell Survival as Criterium.- 3.5.2 Correction for Cell Multiplicity.- 3.5.3 The Shape of the Cell Survival Curve.- 3.5.4 The Analysis of Experimental Data.- 3.6 Variation in the Survival Curve Through the Cell Cycle.- 3.7 Asynchronous Cell Populations.- 3.8 The Experimental Correlation Between Cell Survival and DNA Double Strand Breaks.- 3.9 Summary.- 4. Chromosomal Aberrations.- 4.1 Introduction.- 4.2 The Nature and Yield of Chromosomal Aberrations.- 4.3 The Classical and Exchange Theories of Radiation- Induced Chromosomal Aberrations.- 4.3.1 The Classical Theory.- 4.3.2 The Exchange Theory.- 4.3.3 The Problem.- 4.4 The Molecular Theory of Radiation-Induced Chromosomal Aberrations.- 4.4.1 The Yield of Chromosomal Aberrations.- 4.4.2 The Formation of Chromosomal Aberrations by the Process of Telomere-Break Rejoining.- 4.4.2.1 A Possible Molecular Mechanism for Rejoining Between a Telomere and a Break and the Stabilization of a Broken End.- 4.4.3 The Formation of Chromosomal Aberrations by the Process of Recombinational Rejoining.- 4.4.3.1 Repetitive DNA.- 4.4.3.2 Palindromes.- 4.4.3.3 Incompleteness.- 4.4.4 The Experimental Evidence for Telomere-Break Rejoining.- 4.4.4.1 The Haplopappus Experiment.- 4.4.4.2 Other Radiation Experiments.- 4.4.4.3 Medical Cytology.- 4.4.5 The Experimental Evidence for the Process of Recip--rocal Recombination.- 4.4.6 Two Mechanisms for the Formation of Chromosomal Aberrations?.- 4.4.6.1 The Molecular Nature of the Telomere.- 4.4.6.2 The Role of Caffeine.- 4.5 Complex Chromosomal Rearrangements.- 4.6 Gene Transplantation.- 4.7 Summary.- 5. Somatic Mutations.- 5.1 Point and Chromosome Mutations.- 5.2 Some Molecular Mechanisms Which Could Give Rise to Mutations from DNA Double Strand Breaks.- 5.2.1 The Rejoining of Single Stranded Tails.- 5.2.2 Resnick's Model for Gene Conversion.- 5.2.3 Resnick's Model for Reciprocal Recombination.- 5.2.4 Rejoining Between a Telomere and a Single Stranded Tail.- 5.2.5 No Repair.- 5.2.6 The Repair Processes and Mutation Induction.- 5.3 Mutation Frequency Dose Relationships.- 5.3.1 The Induction of Mutations.- 5.3.2 The Suppression of Mutation Expression.- 5.3.3 The Influence of Cell Killing.- 5.4 The Analysis of Experimental Data.- 5.5 Two Mutations in the Same Cell Population.- 5.6 The Mutation Spectrum.- 5.7 Summary.- 6. Correlations.- 6.1 Introduction.- 6.2 The Survival-Survival Correlation.- 6.3 The Survival-Chromosomal Aberration Correlation.- 6.4 The Correlation Between Different Chromosomal Aberrations.- 6.5 The Correlation Between "Normal" Chromosomal Aberrations and "Complex" Chromosomal Aberrations.- 6.6 The Correlation Between Survival and Somatic Mutation.- 6.7 The Correlation Between Two Different Mutations Induced in the Same Cell Population.- 6.8 The Peak Incidence - an Implied Correlation.- 6.9 What Do the Correlations Mean?.- 7. Repair.- 7.1 Introduction.- 7.2 The Repair of DNA Single Strand Breaks and the Dose Rate Effect.- 7.2.1 Experimental Evidence on DNA Single Strand Break Repair.- 7.2.2 The Time Scale of the Three Dose Rate Regions.- 7.2.3 The Exponential Repair of DNA Single Strand Breaks and Its Effect on the Dose Response Relationships.- 7.2.4 Implications for the InS/D Versus D Analysis.- 7.2.5 Complicated Repair Rates.- 7.2.6 Practical Difficulties in the Determination of Dose-rate Effects.- 7.3 The Repair of DNA Single Strand Breaks and the Effect of Dose Fractionation.- 7.3.1 The Analysis of Repair Using Fractionation Studies.- 7.4 The Repair of DNA Double Strand Breaks and the Post-Irradiation Effect.- 7.4.1 The Quantitative Effect of DNA Double Strand Break Repair on Cell Survival.- 7.4.1.1 The Time Dependence of the Repair of DNA Double Strand Breaks.- 7.4.2 The Quantitative Effect of DNA Double Strand Break Repair on Chromosomal Aberration Yield.- 7.4.3 The Quantitative Effect of DNA Double Strand Break Repair on Mutation Frequency.- 7.4.4 Is the Efficiency for the Repair of DNA Double Strand Breaks Always Dose-independent?.- 7.5 The Difference Between Sub-lethal Damage Repair and Potentially Lethal Damage Repair.- 8. Radiation Quality.- 8.1 The Differing Shape of Dose-response Relationships.- 8.2 A Qualitative Assessment of the Dependence of the ?-Coefficient on Radiation Quality.- 8.3 A Qualitative Assessment of the Dependence of the ?-Coefficient on Radiation Quality.- 8.4 How Constant is the Value of RBEo?.- 8.4.1 The Variation of RBEo in the Cell Cycle.- 8.4.2 The Effect of Different Conditions in the Cell.- 8.4.3 Extremely High Values of RBEo.- 8.5 The Size of the Target.- 8.6 A Calculation of the Dependence of the a- and ss- Coefficients on Radiation Quality.- 8.6.1 The Track Model.- 8.6.2 A Calculation of the Induction of DNA Single and Double Strand Breaks.- 8.6.3 A Quantitative Assessment of the Dependence of Cell Survival on Radiation Quality.- 8.6.4 The Relation Between Physics, Chemistry, and Biology.- 8.7 Summary.- 9. Cancer.- 9.1 Introduction.- 9.2 Somatic Mutation and Cancer.- 9.2.1 Historical Development.- 9.2.2 The Modern Evidence Supporting the Somatic Mutation Theory.- 9.2.2.1 The Mutagen Screening Tests.- 9.2.2.2 The Typical Chromosomal Aberrations.- 9.2.2.3 The Repair-deficient Human Disorders.- 9.3 The Malignant Cell.- 9.4 Radiation-Induced Cell Transformation.- 9.4.1 The Diploid Carrier Cell.- 9.4.2 The Tetraploid Carrier Cell.- 9.4.3 The Diploid Non-Carrier Cell.- 9.5 Extrapolation to Animals and Man.- 9.5.1 Experimental Data for Animals.- 9.5.2 Radiation-induced Malignancy in Man.- 9.5.2.1 Sparsely Ionizing Radiation.- 9.5.2.2 Densely Ionizing Radiation.- 9.6 Conclusion.- 10. Genetic Effects.- 10.1 Introduction.- 10.2 The Induction of Dominant Lethal Mutations.- 10.3 Correlations Between Different Genetic End Points.- 10.3.1 The Correlation Between Dominant Lethality and the Yield of Chromosomal Aberrations.- 10.3.2 The Correlation Between Different Chromosomal Aberrations.- 10.3.3 The Correlation Between Dominant Visible Mutations and Specific Locus Mutations in the Mouse.- 10.3.4 The Correlation Between Dominant and Recessive Lethal Mutations.- 10.4 The Induction of Translocations in the Spermatogonia of the Mouse.- 10.4.1 The Spermatogonial Stem Cell Development.- 10.4.2 Acute Irradiation.- 10.4.3 The Effect of Dose Rate.- 10.4.4 Short-Term Fractionation.- 10.4.5 Twenty-Four-Hour Fractionation.- 10.4.6 Long-Term Fractionation.- 10.5 The Induction of Specific Locus Mutations in the Mouse.- 10.6 Conclusions.- 11. Synergistic Interaction.- 11.1 Introduction.- 11.2 Theoretical Development.- 11.3 Agent Toxicity.- 11.4 Agent Dosimetry.- 11.5 Experimental Examples of Synergism.- 11.5.1 The Interaction of Radiation with UV.- 11.5.2 The Interaction of Radiation with Halogenated Pyrimidine Analogues.- 11.5.3 The Interaction of Radiation with Nitrosourea Compounds.- 11.5.4 The Interaction of Radiation with Diamide.- 11.6 General Discussion.- 12. Implications.- 12.1 Radiological Protection.- 12.1.1 Sparsely Ionizing Radiation.- 12.1.2 Densely Ionizing Radiation.- 12.1.3 Cancer as a Recessive Genetic Character.- 12.1.4 Genetic Effects.- 12.1.5 The Effect of Environmental Mutagens.- 12.2 The Chemical Hazard.- 12.3 Radiation Therapy.- 12.3.1 Fractionation.- 12.3.1.1 ?-Type Sensitizer.- 12.3.1.2 ?-Type Sensitizer.- 12.3.1.3 Implications for the Choice of Sensitizer.- 12.4 Plant Mutation Breeding.- 12.5 Postscript.- References.- List of Abbreviations.
Series Title: Monographs on theoretical and applied genetics, v. 5.
Responsibility: K.H. Chadwick and H.P. Leenhouts.

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