Cell Death in Biology and Pathology

ISBN-13: 9789401169233 / Angielski / Miękka / 2012 / 493 str.

I. Bowen

Opis

It is clear that lysosomal enzymes often play a role in the destruction of the cytoplasm, but very few authorities feel that they initiate the process (Chapters 1, 2, 3, 5 -8, 12, 13). The cells show many forms of damage, and sometimes even complete destruction, before Iysosomes become a dominant part of the environ- ment. What initiates the process is still unclear, although in several instances it appears that the death of a cell may arise from anyone of several pathways (Chapters, 10, II). It is rather interesting that evolution has chosen to achieve the same goal by different means. Apparently no one point is exceptionally or pre- ferentially vulnerable, though a common pathway, such as permeability of the plasma membrane to calcium (Chapter 7), might currently be too subtle for routine identification. Factors which affect membrane stability and which induce mem- brane bending can lead to blebing, cell fragmentation and death. Thus, more work on the changing chemistry of the plasma membrane in relation to environmental fluctuations would be welcomed. Space requirements and the major orientation of the book forced the exclusion of several very interesting topics: an evolutionary treatment of the advantages of cell death as a means of eliminating vestigial organs or embryonic scaffolding; or consider- ation of the merits of body sculpting by cell death rather than cell growth.

Spis treści

1 Cell death: a new classification separating apoptosis from necrosis.- 1.1 Introduction.- 1.2 Necrosis.- 1.2.1 Incidence.- 1.2.2 Morphology.- 1.2.3 Mechanism.- 1.3 Apoptosis.- 1.3.1 Incidence.- 1.3.2 Morphology.- 1.3.3 Mechanism.- 1.4 Validity of the classification.- 1.4.1 Relevance.- 1.4.2 Scope.- 1.4.3 Practicability.- 1.5 Summary and conclusions.- References.- 2 Cell death in embryogenesis.- 2.1 Introduction.- 2.2 Limb development and cell death.- 2.2.1 The areas of cell death.- 2.2.2 The role of cell death.- 2.2.3 Phylogenetic aspects.- 2.2.4 The programming of cell death.- 2.2.5 Genetic control of cell death in the limb bud.- 2.2.6 Teratogenic modification of cell death patterns in limb morphogenesis.- 2.3 Development of the nervous system.- 2.3.1 Neural tube closure.- 2.3.2 The role of the periphery in limb innervation.- 2.4 Differentiation of the reproductive system.- 2.5 Epithelial cell death during fusion of the secondary palate in mammalian development.- 2.6 Lysosomes and the control of embryonic cell death at the cellular level.- References.- 3 Cell death in metamorphosis Richard.- 3.1 Introduction.- 3.2 Amphibian metamorphosis.- 3.2.1 Anuran tail fins.- 3.2.2 Anuran tail muscle.- 3.2.3 Other tail tissues.- 3.2.4 Anuran tissues other than tail.- 3.2.5 Cell death in amphibian metamorphosis: summary.- 3.3 Metamorphosis in invertebrates.- 3.3.1 General comments.- 3.3.2 Insect muscle.- 3.3.3 Other invertebrate tissues.- 3.4 A model of cell death in metamorphosis.- 3.5 Cell death in metamorphosis: the future.- References.- 4 Tissue homeostasis and cell death.- 4.1 Introduction.- 4.2 Growth patterns.- 4.3 Organ growth control.- 4.3.1 Cell number and turnover.- 4.3.2 Control of cell loss and cell death.- 4.4 Model systems — the thymus.- 4.4.1 Autonomy of the thymus.- 4.4.2 Cell death and cell loss in the thymus.- 4.5 Homeostasis in malignant tissue.- 4.5.1 Tumour necrosis.- 4.5.2 Immunological cytolysis and differentiation.- 4.5.3 Autoregulation in tumours.- 4.5.4 Microenvironment of tumours.- 4.5.5 Cancer chemotherapy 138 References.- 5 Cell senescence and death in plants.- 5.1 Introduction.- 5.1.1 Terminology.- 5.1.2 Mechanisms leading to cell death.- 5.1.3 Cell senescence and possible mechanisms.- 5.1.4 Cell senescence and death.- 5.2 Examination of senescent and dying cells.- 5.2.1 Vital dye studies.- 5.2.2 Ultrastructural studies.- 5.3 Biochemical and cytochemical consideration.- 5.4 Possibile interpretations of the biochemical, cytochemical and ultrastructural studies.- 5.4.1 Respiratory control.- 5.4.2 Dispersal of hydrolases.- 5.5 Mechanisms of cell senescence and death revisited.- 5.5.1 The somatic mutation theory.- 5.5.2 Error catastrophe theory.- 5.5.3 Pathological and mechanical damage.- 5.5.4 The timing and markers of the onset of cell death 162 References.- 6 The tissue kinetics of cell loss.- 6.1 Introduction.- 6.2 The cell cycle.- 6.3 The organization of cell populations.- 6.4 The measurement of the kinetics of cell loss.- 6.4.1 Theoretical aspects of the kinetics of cell loss.- 6.4.2 Age-dependent death process.- 6.4.3 Methods for the estimation of loss parameters.- 6.4.4 The assessment of age-dependent loss in tumour cell populations.- 6.4.5 Pitfalls in the assessment of cell loss from growth curves.- 6.4.6 Estimation of cell loss rates from measurements of the turnover of labelled thymidine or thymidine analogues.- 6.4.7 The assessment of clonogenic cell loss.- 6.5 Some examples involving the measurement of cell loss kinetics in normal tissues.- 6.5.1 Differentiation-induced cell loss.- 6.5.2 Cell loss parameters in the adrenal cortex.- 6.5.3 Cell loss in the human epidermis.- 6.5.4 Cell death in the intestinal mucosa.- 6.5.5 Cell death in the prostrate complex.- 6.5.6 The kinetics of cell death in lymphoid tissue.- 6.5.7 Assessment of cell loss in vitro.- 6.6 The kinetics of cell loss in tumours.- 6.6.1 Cell loss in experimental tumours.- 6.6.2 Loss of clonogenic cells in tumours.- 6.7 Tissue responses.- 6.8 Conclusions.- References.- 7 Cell death and the disease process. The role of calcium.- 7.1 Introduction.- 7.2 Stages of cell injury 209 7.2.1 Comments on the stages.- 7.3 Mechanisms of progression.- 7.4 The role of ion shifts in cell injury.- 7.5 Calcium and cell injury.- 7.5.1 Mechanisms.- 7.5.2 Phospholipases.- 7.5.3 Cell shape modifications.- 7.6 Hypothesis.- 7.7 Summary 234 References.- 8 Cell death in vitro.- 8.1 Introduction.- 8.2 Cell aging and death in vitro.- 8.3 Donor age versus cell doubling potential.- 8.4 Species lifespan versus cell doubling potential.- 8.5 The finite lifetime of normal cells transplanted in vivo.- 8.6 Population doublings in vivo.- 8.7 Organ clocks.- 8.8 Clonal variation.- 8.9 Irradiation, DNA repair and effects of visible light.- 8.10 Cytogenetic studies.- 8.11 Error accumulation.- 8.12 The proliferating pool.- 8.13 Efforts to increase population doubling potential.- 8.14 Phase III in cultured mouse fibroblasts.- 8.15 Phase III theories.- 8.16 Can cell death be normal?.- 8.17 Dividing, slowly dividing and non-dividing cells.- 8.18 Aging or differentiation?.- 8.19 Functional and biochemical changes that occur in cultured normal human cells.- 8.20 Immortal cells.- References.- 9 Nucleic acids in cell death.- 9.1 The basic problem.- 9.2 Protein synthesis in eukaryotic cells.- 9.3 Nucleic acids in silk glands.- 9.4 Limitations of present data.- 9.5 Future developments 290 References.- 10 Mechanism(s) of action of nerve growth factor in intact and lethally injured sympathetic nerve cell in neonatal rodents.- 10.1 Introduction.- 10.2 Historical survey.- 10.3 The salivary NGF: morphological and biochemical effects induced in its target cells.- 10.3.1 The 2.5S and 7S NGFs.- 10.3.2 Morphological effects of NGF.- 10.3.3 Metabolic effects of NGF.- 10.3.4 Effects of NGF on catecholamine synthesis.- 10.3.5 Interaction of NGF and contractile fibrillar proteins.- 10.4 Dual access and mechanisms of action of NGF in its target cells.- 10.5 Destruction of immature sympathetic nerve cells by immunochemical, pharmacological and surgical procedures.- 10.5.1 Immunosympathectomy.- 10.5.2 Chemical sympathectomy.- 10.6 Surgical axotomy.- 10.7 Protective effects of NGF against 6-OHDA, guanethidine, vinblastine, AS-NGF and surgical axotomy.- 10.7.1 NGF and 6-OHDA.- 10.7.2 NGF and guanethidine.- 10.7.3 NGF and vinblastine.- 10.7.4 NGF and AS-NGF.- 10.7.5 NGF and surgical axotomy.- 10.8 Some considerations and concluding remarks.- References.- 11 Glucocorticoid-induced lymphocyte death.- 11.1 Introduction.- 11.2 Glucocorticoid receptors and metabolic effects in lymphocytes.- 11.2.1 Rat thymus cells.- 11.2.2 Normal and leukaemic human lymphocytes.- 11.3.3 Lymphoid cell lines.- 11.3 Lethal effects of glucocorticoids on lymphocytes.- 11.3.1 Morphological changes.- 11.3.2 Species variation in sensitivity to killing by glucocorticoids.- 11.3.3 Variation in sensitivity among subpopulations of lymphocytes.- 11.3.4 Effects on malignant lymphocytes.- 11.4 Genetic analysis of glucocorticoid-induced cell death.- 11.4.1 Models for studying the lethal actions of glucocorticoids.- 11.4.2 Glucocorticoid receptors in mutants and other cells resistant to glucocorticoid-induced cell death.- 11.5 Mechanisms of glucocorticoid-induced cell death.- 11.5.1 Relations among early glucocorticoid effects and cell death.- 11.5.2 Indirect effects of glucocorticoids on lymphocytes.- 11.6 Conclusions.- References.- 12 The role of the LT system in cell destruction in vitro.- 12.1 Introduction.- 12.2 Molecular characteristics of the LT systems of cytotoxic effector molecules.- 12.3 Cellular processes involved in LT release by unstimulated (primary) and stimulated (secondary) human lymphocytes.- 12.4 Types of lytic reactions induced by lytic molecules of various weights in vitro.- 12.5 Conclusions.- References.- 13 Techniques for demonstrating cell death.- 13.1 Introduction.- 13.1.1 Programmed cell death.- 13.1.2 Acute cell death.- 13.2 Microscopical.- 13.2.1 Histological.- 13.2.2 Fine-structural.- 13.3 Cytochemical and biochemical.- 13.3.1 Markers of phagocytosis.- 13.3.2 Markers of hydrolysis.- 13.3.4 Other enzymes.- 13.3.5 DNA.- 13.3.6 RNA and synthetic changes.- 13.3.7 Methods related to immune killing.- 13.3.8 Accumulated products 426 13.4 Conclusions.- References.- Author index.