Showing papers on "Apoptosis published in 1979"

Hormonal control of apoptosis in hamster uterine luminal epithelium.

Abstract: The hamster uterine luminal epithelium undergoes cyclic morphological changes, which include mitosis and hypertrophy prior to ovulation and degenerative changes after ovulation. We have previously shown that the degenerative changes are symptoms of estradiol (E2) withdrawal; they occur within 24 hours after ovariectomy, can be prevented by E2 treatment, and are associated with a decline in the content of uterine nuclear E2 receptor (West et al., 1978). In this report, the results of an electron microscopic study of the uterine luminal epithelium in cycling and hormonally altered hamsters are described. During estrus and after ovariectomy, the death of numerous epithelial cells occurs by apoptosis. The ultrastructural alterations in such cells include condensation and margination of the chromatin, cytoplasmic condensation, amoeboid changes in cell shape with formation of pseudopodial extensions, and nuclear and cytoplasmic fragmentation. The cell fragments, or apoptotic bodies, accumulate near the basal lamina, and are then phagocytosed by macrophages, and possibly by neutrophils as well. The ultrastructural features of cell death by apoptosis in the hamster uterus are similar to those observed by others in a variety of tissues. Because of the periodic, hormonally regulated occurrence of extensive apoptosis in the hamster uterine epithelium during the estrous cycle, this system is well-suited for further investigations on the ultrastructural alterations that occur in cells undergoing apoptosis. In addition, apoptosis appears to be a sensitive morphological endpoint of E2 withdrawal in the hamster uterine luminal epithelium.

Non-immunological cell death of intravenously injected murine tumour cells.

Abstract: Most DBA mastocytoma and Sarcoma 180 cells trapped in the lungs of mice after i.v. injection died within 7 h. Rates of cell death were similar for both tumour cell lines. Rates of tumour cell death were unrelated to whether the cells were allogeneic or syngeneic, induced platelet aggregation or not, had different patterns of subsequent tumour growth, or were injected in varying numbers. Cell death was by coagulative necrosis, not apoptosis. Sarcoma 180 tumour cells were quickly localized in the lung and enclosed in platelet aggregates which remained, with degranulation, until the time of tumour cell death. However, platelet aggregation did not appear to play a role in tumour cell killing. The prevention of platelet aggregation by pretreatment of mice with an anticoagulant had little effect on the rate of death of tumour cells in the lung. Mastocytoma tumour cells did not cause platelet aggregation, yet died in the lung at similar rates to Sarcoma 180 cells. The killing of tumour cells in the lung did not appear to be cell-mediated. No mononuclear cells were seen in the vicinity of tumour cells and the type of cell death was not that associated with cell-mediated killing. The tumour cells did not die within 6 h of being injected into the peritoneal cavity. It is suggested that a nonspecific non-immunological process results in the death of intravenously injected tumour cells in the lung. This process was not affected by differing oxygen levels in the inhaled gas.

Apoptosis: A Distinctive Mode of Cell Death that Plays an Opposite Role to Mitosis in Cell Population Kinetics

Abstract: The term apoptosis has been coined for a morphologically distinctive mode of cell death, which plays an opposite role to mitosis in controlling the size of animal tissues: it is fundamentally different from the well known phenomenon of necrosis that results from irreversible injury to cells by agents such as toxins and ischaemia. Cells affected by apoptosis condense and bud to produce many membrane‐bounded fragments in which organelles are well preserved. These are phagocytosed and digested by nearby resident tissue cells without associated inflammation; the viable cells merely close ranks. Extensive deletion of cells may thus take place without disorganisation of overall tissue architecture. Apoptosis occurs continuously in healthy animals. It is enhanced in endocrine‐dependent tissues during the reversible shrinkage that follows appropriate hormone withdrawal or administration, and it is also implicated in total and irreversible involution of tissues in normal animals, such as loss of the tadpole tail during metamorphosis and elimination of phylogenetic vestiges during embryonic development. Apoptosis takes place spontaneously and continuously in malignant neoplasms, often grossly retarding their growth, and cytotoxic drug administration and X irradiation enhance apoptosis as well as inhibiting mitosis in neoplasms; tumour regression following therapy with these agents is the result of tipping the balance between the two processes. Hyperthermia enhances apoptosis in foetal tissues and adult seminiferous tubules; its effect on apoptosis in neoplasms needs study. Cell mediated immune attack on cells induces apoptosis, not necrosis; apoptosis may thus sometimes be enhanced in neoplasms by immunological means. The features of apoptosis suggest that it is an active process of cellular self‐destruction rather than a form of cell degeneration. This carries the implication that it is genetically programmed. Further understanding of the regulation of the onset of apoptosis at the molecular level may lead to the discovery of improved methods of tumour treatment.