Historical Aspects of Physiological Cell Death Prior to Description of Apoptosis
Cell death as a physiological process was recognized in the early 1920’s. There is a large and rich literature on cell death in hematopoiesis, embryogenesis, immunology, cancer, after exposure of lymphocytes to ionizing radiation or cortisone. Cell death and its measurement has been an essential component in study of cell kinetics of all tissues in which cell turnover is evident.
The objective of this concise and incomplete review on cell death, prior to emergence of the term apoptosis, was to document that non-necrotic cell death in normal and pathologic processes has been appreciated for several decades. When it was discovered that several tissues in the adult continued to have mitoses and that with each mitosis there was a net gain of one cell it was self-evident that there had to be a compensatory loss of cells by death, a process which might appropriately be called cytocide.
Cells are programmed to die in order to fashion organs during embryogenesis, to allow the development of the immune system, to maintain homeostasis in the endocrine-dependent tissues, to limit reactive hyperplasia, or to maintain a steady state in self-renewing tissues in addition to differentiation. Cell death is also a pathophysiological mechanism by which normal and malignant cells may die in response to ionizing radiation and/or chemotherapeutic drugs and toxic chemicals. In the landmark publication in 1972 by Kerr et al. (1) the term apoptosis was coined to dignify the phenomenon of cell death. After the coining of the name apoptosis and its cytological description and subsequently the identification of its genetic controls, opened the flood gates for a torrent of publications on apoptosis. There were eight publications in 1980 and 800 in 1993. Publications continued to expand in ’94 and’95.
KeywordsChronic Lymphocytic Leukemia Tritiated Thymidine Historical Aspect Compensatory Loss Clonal Selection Theory
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- 2.Sabin FR, Cunningham RS, Doan CA, Kindawall JA: The normal rhythm of the white blood cells. Bulletin of the Johns Hopkins Hospital 37: 14, 1925Google Scholar
- 6.Maloney MA, Patt HM, Lund JE: Granulocyte dynamics and a question of ineffective granulopoiesis. Cell Tissue Kinetics 4: 201, 1971Google Scholar
- 7.JamuarN, Cronkite EP: The fate of blood granulocytes. Exp. Hemat. 8: 884, 1980Google Scholar
- 11.Trowell CA: The action of cortisone on lymphocytes in vitro. J. of Physiology 119: 274, 1953Google Scholar
- 13.Cronkite EP, Fliedner TM, Killman SA, Rubini JR: Tritium-labeled thymidine: its somatic toxicity and use in the study of growth rates and potential in normal and malignant tissue of man and animals, in Tritium in the Physical and Biological Sciences, vol 2. International Atomic Energy Agency, Vienna, 1962, p 189Google Scholar
- 14.Burnet M: The clonal selection theory of acquired immunity. Vanderbilt University Press, Nashville, 1959, p58Google Scholar
- 16.Stohlman Jr F: Observations on the Kinetics of Red Cell production, in Kinetics of Cellular Prolifration, Grune and Stratton, NY, 1959, p 318Google Scholar
- 19.Killman SA, Cronkite EP, Fliedner TM, Bond VP: Cell proliferation in multiple myeloma studied with tritiated thymidine in vivo. Laboratory Investigation 11: 845, 1962Google Scholar
- 23.Leblond CP, Walker DE: Renewal of cell populations. Physiological Reviews 36: 235, 1956Google Scholar
- 24.Johnson HA: Some problems associated with histological study of cell proliferation kinetics. Cytologia 26: 32, 1961Google Scholar
- 25.Cronkite EP: Enigmas underlying the study of hematopoietic cell proliferation. Fed. Proc. 23: 649, 1964Google Scholar
- 26.Tornei L David, Frederick O. Cope Frederick O (eds): Apoptosis: The molecular basis of cell death. Current Communications in Cell and Molecular Biology. Cold Spring Harbor Laboratory Press, 1991.Google Scholar