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Programmed Cell Death/Apoptosis. Historical background of the discovery of the stereotypical internucleosomal fragmentation of chromatine DNA as a hallmark of apoptosis. The discovery of the stereotypical internucleosomal degradation of genomic DNA (lymphocytes, thymocytes etc.) to a regular repeating oligonucleosomal fragments generated by Ca/Mg-dependent endonuclease is accepted as a fundamental compound and one of the best-characterized biochemical marker of the process that called in molecular and cellular biology apoptosis/programmed cell death.Apoptosis is a wide spread phenomenon and a basic physiological process that accounts for homeostasis in normal tissues and malignant neoplasms,cell mediating immune killing, for cell death induced by physiological stimuli or their withdrawal and for cell death triggered by several agents during cancer treatment. In 1951 Glucksmann A. described on morphological grounds evidence characterizing selective death as a normal process of embryonic development. In 1964-1965 Lokshin R.A. And Williams C.M. referred to this process as a programmed cell death in recognition of “timing and synchrony involved”. In 1970 Williamson R.   described that cytoplasmic DNA isolated from mouse liver cells after culture is characterized with a fragments of a series of multiples of a  unit molecular weight of 135000 Dalton,consistent with a hypothesis that these DNA fragments are specific degradation product of nuclear DNA. In 1972 Kerr J.,Wyllie A. and Currie A. described on morphological grounds the features of a programmed cell death/apoptosis  which exhibits specific morphological characteristics distinctly different from necrosis. In 1973 Hewish D.R. And Burgoyne L.A. in the context of study of subchromatin structure found that chromatin is accessible to the Ca++/Mg++  endonuclease with formation of digest product with a regular series of molecular weight  similar to the previously described by Williamson R.                                  In 1974 Williams J.R. ,Little J.B.,Shipley W. U. using cells exposed to widely differing type of trauma  found,that during cell death degraded DNA in “every case had a modal value of between 10(x6) and10(x7) Dalton and cellular metabolism is required  to produce degradation of DNA”. However this observation was without indication “whether the incision attack on the DNA molecule was a random or rather at particular site,that have structural or functional meaning”. In 1976 Scalka M., Matyasova M, Cejkova M. described  internucleosomal fragmentation of irradiated lymphoid chromatin DNA in vivo. Six year passed from 1972 to 1978/1980 until discovery and evaluation of internucleosomal fragmentation of DNA during apoptotic cell death as a hallmark of apoptosis. Since 1972 (Kerr J., Wyllie A., and Currie A.) it is accepted that glucocorticoids induced death of lymphocytes belongs to the apoptosis. In 1978 Zakharyan Robert A., Pogosian R. originally presented paper revealing that glucocorticoids  induced DNA degradation in rat lymphoid tissue in thymus and spleen   occurred in a specific pattern producing fragments of DNA electrophoretically similar to those observed after treatment of chromatin with microccoccal nuclease ,which indicated internucleosomal cleavege pattern of DNA degradation  occurred during apoptosis. Thus,the first link between programmed cell death/apoptosis and  internucleosomal fragmentation of chromatin DNA was discovered and soon became as a specific feature of apoptosis. In 1980 Wyllie A. reported additional evidence for occurring internucleosomal DNA cleavage pattern as a specific feature in glucocorticoid treated thymocytes undergoing apoptosis. Internucleosomal DNA cleavage pattern was observed as a specific feature of apoptosis in 1978/1980  and became as a hallmark of programmed cell death  and ERA of apoptosis in molecular and cellular  biology was started. REFERENCES: GLUCKSMANN, A. (1951). Cell deaths in normal vertebrate ontogeny. Biol.Rev..Cambridge,.Phil.Soc.,26,59-86. LOCKSHIN, R. A., and WILLIAMS, C. M. (1964). Programmed cell death. I. J. Insect. Physiol. 10, 643-649. LOCKSHIN, R. A., and WILLIAMS, C. M. (1965a J. Programmed cell death. II. J. Insect. Physiol. 11, 123-133. LOCKSHIN, R. A., and WILLIAMS. C. M. (1965b J. Programmed cell death. III. J. Insect. Physiol. 11,601-610. WILLIAMSON ROBERT.(1970) .Properties of Rapidly Labeled Deoxyribonucleic Acid Fragments Isolated from the Cytoplasm of Primary Cultures of Embryonic Mouse Liver Cells. Mol. Biol. 51, 157-168 .  Kerr JF, Wyllie AH, Currie AR. (1972). Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br. J. Cancer 26:239–57. Dean R. Hewish  and Leigh  A. Burgoyne (1973 ).CHROMATIN SUB-STRUCTURE. THE DIGESTION OF CHROMATIN DNA AT REGULARLY SPACED SITES   BY  A  NUCLEAR DEOXYRIBONUCLEASE. BIOCHEMICAL  AND  BIOPHYSICAL    RESEARCH COMMUNICATIONS,Vol. 52, No. 2, 157-168. Williams J.R.,Little J.B., Shipley W.,U. (1974).Association of mammalian cell death with a specific endonucleolytic degradation of DNA. Nature 252,754-755. Skalka M., Matyasova J., Ceskova M .(1976). DNA in chromatin of irradiated lymphoid tissues degradation in vivo into regular fragments. FEBS Lett. 72,2,271.                   Zakharyan R.A.,Pogosian R.G.(1978),Glucocorticoid induction of the degradation of lymphocyte chromatin DNA into regularly repeating fragments in vivo. USSR. Doklady Akademii Nauk Armyanskoi SSR(1978),67(2),110-114. CODEN: DANAAW ISSN: 0366-8606.Journal written in Russian. CAN 90:115643 AN 1979:115643  CAPLUS (Copyright 2003 ACS).Chemical Abstracts v.90,1979;90:115643n p.112. Wyllie A.H.(1980). Glucocorticoid-induced thymocyte apoptosis  is associated with endogenous  endonuclease activation. Nature 284:555–556. See also: CORCORAN GB, FIX L, JONES DP, et al., APOPTOSIS - MOLECULAR CONTROL POINT IN TOXICITY. TOXICOLOGY AND APPLIED PHARMACOLOGY 128 (2): 169-181 OCT 1994. WALKER PR, PANDEY S, SIKORSKA M, DEGRADATION OF CHROMATIN IN APOPTOTIC CELLS. CELL DEATH AND DIFFERENTIATION 2 (2): 97-104 APR 1995. WALKER PR, SIKORSKA M, ENDONUCLEASE ACTIVITIES, CHROMATIN STRUCTURE, AND DNA-DEGRADATION IN APOPTOSIS. BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE 72 (11-12): 615-623 NOV-DEC 1994. PANDEY S, WALKER PR, SIKORSKA M, SEPARATE POOLS OF ENDONUCLEASE ACTIVITY ARE RESPONSIBLE FOR INTERNUCLEOSOMAL AND HIGH-MOLECULAR-MASS DNA FRAGMENTATION DURING APOPTOSIS, BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE 72 (11-12): 625-629 ,NOV-DEC, 1994. MINOZ E, MARCOS A, UNZAGA MT, EFFECT OF PROTEIN-DEFICIENCY ON THE LYSOSOMAL ENZYME-ACTIVITIES OF THE SPLEEN AND THYMUS OF WEANLING RATS. JOURNAL OF NUTRITION ): 2133-2141, 1981. Varela,P.; Marcos, A. and Rey de Viñas, J.L. (1985). Effect of cortisol treatment in pregnant rats, on cellular growth of progeny. IRCS Medical Science, 13, 412-413.