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Cell deletion by apoptosis during regression of rat parotid sialadenosis

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Abstract

Enlargement of the rat parotid salivary glands was induced by repeated administration of isoproterenol. Mean wet weights of the treated glands increased steadily to 240% of control values. Following withdrawal of the drug, quantitative histological techniques were used to investigate the balance between hypertrophy, hyperplasia and apoptosis. The volume occupied by acinar cells relative to the total gland volume together with cytoplasmic|:|nuclear area ratios as measures of hypertrophy increased during the early experimental period. Similarly, serous acinar cell mitotic counts increased, indicating that hyperplasia had occurred. Apoptosis was demonstrated at light microscopical level to be the main mechanism for cell deletion as the glands returned to normal size and weight. The results indicate that hypertrophy and hyperplasia of serous acinar cells contribute to isoproterenol-induced sialadenosis. The experimental animal model demonstrates that these proliferative changes are completed by 48 h and thereafter are balanced by apoptosis as the glands recover their normal size and weight.

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References

  1. Adi MM, Chisholm DM, Waterhouse JP (1994) Stereological and immunohistochemical study of development of human fetal labial salivary glands and their S-100 protein reactivity. J Oral Pathol Med 23:36–40

    Google Scholar 

  2. Aherne WA, Dunnill MS (1982). Morphometry. Edward Arnold, London

    Google Scholar 

  3. Alison MR, Sarraf CE (1992) Apoptosis: a gene-directed programme of cell death. R Coll Phys Lond 26:25–35

    Google Scholar 

  4. Ansari B, Coates PJ, Greenstein BD, Hall PA (1993) In-situ end-labelling detects DNA strand breaks in apoptosis and other physiological and pathological states. J Pathol (Lond) 170:1–8

    Google Scholar 

  5. Barka T (1965) Stimulation of DNA synthesis by isoproterenol in the salivary gland. Exp Cell Res 39:355–364

    Google Scholar 

  6. Barka T (1966) Stimulation of RNA synthesis in salivary glands by isoproterenol. Exp Cell Res 41:573–579

    Google Scholar 

  7. Barka T, Burke TG (1977) Secretory behaviour of hypertrophic and hyperplastic salivary glands. Histochem J 9:353–466

    Google Scholar 

  8. Baserga R, Heffler S (1967) Stimulation of DNA synthesis by isoproterenol and its inhibition by actinomycin D. Exp Cell Res 46:571–586

    Google Scholar 

  9. Bogart BI (1975) Secretory dynamics of the rat submaxillary gland: an ultrastructural and cytochemical study of the isoproterenol-induced secretory cycle. J Ultrastruct Res 52:139–155

    Google Scholar 

  10. Boshell JL, Pennington C (1980) Histological observations on the effects of isoproterenol on regenerating submandibular glands of the rat. Cell Tissue Res 213:411–416

    Google Scholar 

  11. Cohen JJ, Duke RC, Fadok VA, Sellins KS (1992) Apoptosis and programmed cell death in immunity. Annu Rev Immunol 10:267–293

    Google Scholar 

  12. Columbano A, Ledda-Columbano GM, Coni PP, Faa G, Liguori C, Santa Cruz G, Pani P (1985) Occurrence of cell death (apoptosis) during the involution of liver hyperplasia. Lab Invest 52:670–675

    Google Scholar 

  13. Dexter TM, Raff MC, Wyllie AH (1994) Death from inside out: the role of apoptosis in development, tissue homeostasis and malignancy. Phil Trans R Soc Lond B 345:231–333

    Google Scholar 

  14. Donath K, Feustel P, Seifert G (1971) Ultrastructural changes of the acini of the salivary glands following experimental administration of ethionine. Virchows Arch [A] 353:360–374

    Google Scholar 

  15. Dunnill MS (1968) Quantitative methods in histology. (Recent advances in clinical pathology, series V). Churchill, London

    Google Scholar 

  16. Dunnill MS (1972) Quantitation in morbid anatomy. Proc R Soc Med 65:537–539

    Google Scholar 

  17. Elias H, Henning A, Schwartz DE (1971) Stereology: applications to biomedical research. Physiol Rev 51:158–200

    Google Scholar 

  18. Garrieli Y, Sherman Y, Ben-Sasson SA (1992) Identification of programmed cell death in situ via specific labelling of nuclear DNA fragmentation. J Cell Biol 119:493–501

    Article  CAS  PubMed  Google Scholar 

  19. Han SS (1967) An electron microscope and radioautographic study of the rat parotid gland after actinomycin D administration. Am J Anat 120:161–184

    Google Scholar 

  20. Hockenbery DM, Nunez G, Milliman C, Schreiber RD, Korosmeyer SJ (1990) Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death. Nature 348:334–336

    Article  CAS  PubMed  Google Scholar 

  21. Jacobson MD, Raff MC (1995) Programmed cell death and bcl-2 protection in very low oxygen. Nature 374:814–816

    Google Scholar 

  22. Jacobson MD, Burne JF, King MP, Miyashita T, Reed JC, Raff MC (1993) Bcl-2 blocks apoptosis in cells lacking mitochondrial DNA. Nature 361:365–369

    Google Scholar 

  23. Merz WA, Schenk RK (1970) Quantitative structural analysis of human cancellous bone. Acta Anat 75:54–66

    Google Scholar 

  24. Novi AM, Baserga R (1971) Association of hypertrophy and DNA synthesis in mouse salivary glands after chronic administration of isoproterenol. Am J Pathol 62:295–307

    Google Scholar 

  25. Parks HF (1961) On the fine structure of the parotid gland of mouse and rat. Am J Anat 108:303–329

    Google Scholar 

  26. Pohto P (1966) Catecholamine-induced salivary gland enlargement in rats. Acta Odontol Scand 24 [Suppl 45]:1–73

    Google Scholar 

  27. Radley JM (1967) Changes in ploidy in the rat submaxillary glands induced by isoprenaline. Exp Cell Res 48:679–681

    Google Scholar 

  28. Rao SM, Yeldandi AV, Subbarao V, Reddy JK (1993) Role of apoptosis in copper deficiency-induced pancreatic involution in the rat. Am J Pathol 142:1952–1957

    Google Scholar 

  29. Redman RS, Sreebny LM (1970) Proliferative behaviour of differentiating cells in the developing rat parotid gland. J Cell Biol 46:81–87

    Google Scholar 

  30. Rutberg U (1961) Ultrastructure and secretory mechanism of the parotid gland. Acta Odontol Scand 19 [Suppl 30] 11–69

    Google Scholar 

  31. Schneyer CA, Finley WH, Finley SC (1967) Increased chromosome number of rat parotid cells after isoproterenol. Proc Soc Exp Biol Med 125:722–728

    Google Scholar 

  32. Schneyer CA, Shackleford JM (1963) Accelerated development of salivary glands of early postnatal rats following isoproterenol. Proc Soc Exp Biol Med 112:320–324

    Google Scholar 

  33. Scott J (1977) Quantitative age changes in the histological structure of human submandibular salivary glands. Arch Oral Biol 22:221–227

    Google Scholar 

  34. Scott J, Gradwell E (1989) A quantitative study of the effects of chronic hypoxia on the histological structure of the rat major salivary glands. Arch Oral Biol 34:315–319

    Google Scholar 

  35. Seifert G (1967) Experimental sialadenitis by isoproterenol and other agents: histochemistry and electronmicroscopy. In: Schneyer LH, Schneyer CA (eds) Secretory mechanisms of salivary glands. Academic Press, New York, pp 191–208

    Google Scholar 

  36. Selye H, Veilleux R, Cantin M (1961) Excessive stimulation of salivary gland growth by isoproterenol. Science 133:44–45

    Google Scholar 

  37. Shannon IL, Chauncey HH (1967) Hyperhydration and parotid flow in man. J Dent Res 46:1028–1031

    Google Scholar 

  38. Shimizu S, Eguchi Y, Kosaka H, Kamiike W, Matsuda H, Tsujimoto Y (1995) Prevention of hypoxia-induced cell death by bcl-2 and bcl-xl. Nature 374:811–813

    Google Scholar 

  39. Takahama M, Barka T (1967) Electron microscopic alteration of the submaxillary gland produced by isoproterenol. J Ultrastruct Res 17:452–474

    Google Scholar 

  40. Tomei AD, Cope FO (1991) Apoptosis: the molecular basis of cell death. (Current communications in cell and molecular biology, no 3) Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY

    Google Scholar 

  41. Walker NI, Gobé GC (1987) Cell death and cell proliferation during atrophy of the rat parotid gland induced by duct obstruction. J Pathol (Lond) 153:334–345

    Google Scholar 

  42. Walker NI, Winterford CM, Williamson RM, Kerr JF (1993) Ethionine-induced atrophy of rat pancreas involves apoptosis of acinar cells. Pancreas 8:443–449

    Google Scholar 

  43. Waterhouse JP, Chisholm DM, Winter RB, Patel M, Yale RS (1973) Replacement of functional parenchymal cells by fat and connective tissue in human submandibular salivary glands: an age-related change. J Oral Pathol 2:16–27

    Google Scholar 

  44. Wilborn WH, Schneyer CA (1970) Ultrastructural changes in rat parotid glands induced by a diet of liquid Metrecal. Z Zellforsch 103:1–11

    Google Scholar 

  45. Wyllie AH (1993) Apoptosis (The 1992 Frank Rose Memorial Lecture). Br J Cancer 67:205–208

    Google Scholar 

  46. Wyllie AH, Kerr JFR, Currie AR (1980) Cell death: the significance of apoptosis. Int Rev Cytol 68:251–306

    CAS  PubMed  Google Scholar 

  47. Young JA, Lennep EW van (1978) The morphology of salivary glands. Academic Press, London)

    Google Scholar 

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Chisholm, D.M., Adi, M.M., Ervine, I.M. et al. Cell deletion by apoptosis during regression of rat parotid sialadenosis. Vichows Archiv A Pathol Anat 427, 181–186 (1995). https://doi.org/10.1007/BF00196524

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  • DOI: https://doi.org/10.1007/BF00196524

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