1 Detection of Effects of Mutagens in Human Populations.- 1. Introduction.- 2. Monitoring Progeny for Evidence of Germ-Cell Mutations.- 2.1. The Classical Approach: Phenotypic Monitoring.- 2.2. Monitoring for Changes in Gene Products.- 3. Detection of Gene Mutations in Somatic Cells.- 3.1. Drug-Resistant Lymphocytes.- 3.2. Hemoglobin Variants.- 4. Nongenetic Indicators of Mutagen Exposure.- 4.1. Alkylation of Proteins.- 4.2. DNA Damage.- 5. Testing for Mutagenic Substances in Body Fluids.- 6. Detection of Altered Sperm.- 6.1. Morphological Sperm Abnormalities.- 6.2. Double Y Bodies in Sperm.- 6.3. Gene Mutations in Sperm.- 7. Summary.- 8. References.- 2 The Use of Intact Cellular Activation Systems in Genetic Toxicology Assays.- 1. Introduction.- 2. Mammalian Cell Mutagenesis.- 2.1. Fibroblast-Mediated Mutagenesis.- 2.2. Hepatocyte-Mediated Mutagenesis.- 2.3. Target Organ and Cell Type Specificities.- 2.4. Studies Using Human Cells.- 3. Bacterial Mutagenesis.- 4. Sister Chromatid Exchange and Chromosome Aberrations.- 5. Cell-Mediated Transformation.- 6. Cytotoxicity and Nucleic Acid Interactions.- 7. Discussion.- 8. Summary.- 9. References.- 3 The Mouse Spot Test As a Predictor of Heritable Genetic Damage and Other Endpoints.- 1. Introduction.- 2. Relation to Measures of Heritable Mutations.- 2.1. Genetic Comparisons.- 2.2. Calculation of “Unit” Mutation Rates.- 2.3. Quantitative Comparisons of SLT and MST Results.- 3. Relation to Other Endpoints.- 4. Summary.- 5. References.- 4 The Bone Marrow Micronucleus Assay: Rationale for a Revised Protocol.- 1. Introduction.- 2. Kinetics of Erythropoiesis.- 3. Rationale for the Basic Aspects of the Protocol.- 3.1. Treatment Regimen.- 3.2. Sample Intervals.- 4. Protocol.- 4.1. General Approach.- 4.2. Protocol Specifics.- 4.3. Spindle Poisons.- 5. Statistical Analysis.- 6. Conclusions.- 7. References.- 5 Relationships between the Chemical Structure and Mutagenic Activity of Monocyclic Aromatic Amines.- 1. Introduction.- 2. Bacterial Strains.- 3. Experimental Methods.- 4. Chemicals.- 5. Mutagenicity Data and Their Interpretation.- 5.1. The 2,4-Diaminoalkoxybenzenes.- 5.2. m-Diaminobenzene and Its 2,4-Diaminoalkylbenzene Derivatives.- 5.3. Nitro-p-phenylenediamine Derivatives.- 5.4. The 3-Amino-4-nitrophenols and the 4-Amino-3- nitrophenols.- 6. Possible Pitfalls in Studies of Structure-Activity Relationships.- 7. Conclusions.- 8. References.- 6 The Measurement of Recessive Lethal Mutations in the Mouse.- 1. Introduction.- 2. Haldane’s Method of Detecting Lethals.- 3. The Backcross Method of Detecting Lethals.- 3.1. Choice of Animals for Studies.- 3.2. Treatment and Breeding Schedule.- 3.3. Identification of Translocation Bearers.- 3.4. The Backcross Matings.- 3.5. Controls.- 4. Irradiation Treatment of Male Germ Cells.- 5. Irradiation Treatment of Female Germ Cells.- 6. Chemical Mutagen Induction of Recessive Lethal Mutations.- 7. Dominant Effects of Recessive Lethal Mutations.- 8. Conclusions.- 9. References.- 7 Chemically Induced Changes in Sperm in Animals and Humans.- 1. Introduction.- 2. The F0 Mouse Sperm Head Morphology Assay.- 2.1. Reproducibility between Laboratories.- 2.2. Results.- 2.3. Method Development.- 3. The F1 Sperm Head Morphology Assay.- 3.1. Genetic Basis of F1 Mouse Sperm Head Morphology Assay.- 3.2. Results.- 3.3. The Potential of the F1 Assay.- 4. Induced Sperm Abnormalities in Humans.- 4.1. Assays Used in the Evaluation of Human Sperm.- 4.2. Comparison of Human and Animal Semen Quality.- 4.3. The Uses of Semen Analysis in Humans.- 5. Implications of Alterations in Human Sperm Quality.- 5.1. Reproductive Implications.- 5.2. Mutagenic Implications.- 5.3. Carcinogenicity Implications.- 6. The Advantages of Sperm Assays.- 7. Recommendations for Future Research and Development.- 8. References.- 8 Mutational Analysis in Cultured Human-Hamster Hybrid Cells.- 1. Introduction.- 2. Origin of Specific Lethal Antisera and Human-Hamster Hybrid Cells.- 2.1. Demonstration of Antisera Specificity.- 2.2. Preparation of Human—Hamster Hybrid Cells Containing Specific Human Chromosomes.- 3. Characterization of the AL Hybrid.- 3.1. Origin of the AL Hybrid.- 3.2. Assignment of the AL Surface Antigens to Human Chromosome 11.- 3.3. Analysis of the AL Antigenic System: Demonstration That the AL Antigenic System Is Composed of a Subset of Activities a1, a2, and a3.- 3.4. Regional Gene Mapping of Markers on Human Chromosome 11.- 3.5. Complementation Analysis of the AL Markers.- 3.6. Biochemical Characterization of the a1 Surface Antigen.- 4. Mutation Studies.- 4.1. Source of Antisera and Complement.- 4.2. Treatment of AL Cells with Suspected Mutagens.- 4.3. Scoring Loss of the a1+ Surface Marker.- 4.4. Yield of a1? Mutants.- 4.5. Fluctuation Analysis for Spontaneous Loss of a1+.- 4.6. Analysis of Induced Loss of Other Markers from Chromosome 11.- 4.7. Production of Mutations by Colcemid.- 5. Conclusions.- 6. References.- 9 Genetic Toxicology of Some Known or Suspected Human Carcinogens.- 1. Introduction.- 2. Chemical Selection.- 3. Method of Literature Review.- 4. Results.- 5. Discussion.- 5.1. Human Respiratory Tract Carcinogens.- 5.2. Human Hematolymphopoietic System Carcinogens.- 5.3. Human Bladder Carcinogens.- 5.4. Human Liver Carcinogens.- 5.5. Other Human Carcinogens or Suspected Human Carcinogens.- 6. Summary and Conclusions.- 7. Appendix: Complete Data Base.- 8. References.- 10 Control of Commercial Chemicals: The Sixth Amendment to the Directive on Dangerous Chemical Substances (79/83 I/EEC) Adopted by the Council of the European Communities.- 1. Introduction.- 2. Text of the Sixth Amendment to the Directive on Dangerous Chemical Substances Adopted by the Council of the European Communities.- 3. References.
