Abstract
Aging may reflect, in part, the outcome of environmental stresses on cells and tissues; a question of major interest, however, is whether a mechanism independent of the environment exists at the cellular level and operates in such a manner that senescence and death are the programmed destiny of normal mammalian cells and tissues. A model system which allows an approach to some aspects of this question is provided by the diploid human cell lines [1,2]. During serial subcultivation these cells retain many of the characteristics of normal cells in situ, such as a stable diploid karyotype and sex chromatin in the interphase nuclei of female cells. In addition, it is now well established that these normal cells will proliferate in culture for varying, but finite periods of time; and that following a period of rapid and vigorous. proliferation, the growth of the population slows down, the cells become granular, debris accumulates, and ultimately, the culture degenerates.
Supported, in part, by U.S. Public Health Service Research Grant R01-HD 02721 from the National Institute of Child Health and Human Development and Pa. Dept. of Health Contract 69–593–1, ME-561 from the Commonwealth of Pennsylvania.
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Cristofalo, V.J. (1970). Metabolic Aspects of Aging in Diploid Human Cells. In: Holečková, E., Cristofalo, V.J. (eds) Aging in Cell and Tissue Culture. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1821-7_6
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DOI: https://doi.org/10.1007/978-1-4684-1821-7_6
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