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Glycogen and endoplasmic reticulum of the liver cell after high doses of the carcinogen N-nitrosomorpholin [Glykogen und endoplasmatisches Reticulum der Leberzelle nach hohen Dosen des Carcinogens N-Nitrosomorpholin]

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Glycogen and endoplasmic reticulum of the liver cell after high doses of the carcinogen N-nitrosomorpholin [Glykogen und endoplasmatisches Reticulum der Leberzelle nach hohen Dosen des Carcinogens N-Nitrosomorpholin]
Theodossiou, A. Bannasch, P. Reuss, W.
scientific_publication_article
Επιστημονική δημοσίευση - Άρθρο Περιοδικού (EL)
Scientific publication - Journal Article (EN)
1971
The effect of high doses of the carcinogen NNM on hepatocellular fine structure is analyzed in rats by means of light and electron microscopy. Alterations of the 3 cytoplasmic components: glycogen-endoplasmic reticulum (ER)-ribosomes predominate. During carcinogen application nearly all hepatocytes show a pronounced loss of glycogen. At the same time the ER and the ribosomes undergo fairly different changes. There are 4 basic reactions: 1. ER-disorganization, 2. ER-proliferation, 3. ribosomal reduction, 4. ribosomal enhancement. The disorganization of the ER may be linked with a general reduction of ribosomes or with an enhancement of free ribosomes and helical arrangement of polysomes. The newly formed ER seems always to be agranular initially. It is often transformed, however, into atypical granular reticulum. Cells deficient in ribosomes and glycogen mostly undergo coagulation necrosis, always leading to a marked loss of parenchyma. Cells rich in ribosomes, on the other hand, frequently show mitoses which, as a rule, are abnormal. This explains the development of polyploid nuclei and partly also the increase in cytoplasmic volume of numerous ribosome-rich cells. After with drawal of the carcinogen ribosomal enhancement, glycogen loss and increase in mitotic rate proove to be reversible within 5 weeks. Thus these cellular alterations should not be considered precancerous lesions. They probably indicate incomplete regeneration processes, initiated by toxic necrosis, disturbed, however, by the intoxication itself. © 1971 Springer-Verlag. (EN)
Ερευνητικό υλικό ΕΚΠΑ
https://creativecommons.org/licenses/by-nc/4.0/
University of Athens
Pergamos Digital Library
Journal Article



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