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Mechanisms of adaptation of hepatocytes to chronic hypo thyroidism a cyto photometric and morphometric study



Mechanisms of adaptation of hepatocytes to chronic hypo thyroidism a cyto photometric and morphometric study



Pathology Research and Practice 162(4): 398-419



The quantitative cytoarchitecture of liver parenchymal cells is influenced by hormones of the thyroid gland. They enhance the membrane synthesis of the mitochondria and of the endoplasmic reticulum. Liver parenchyma cells [20 Wistar rats] were analyzed morphometrically 6 mo. after thyroidectomy to study the process of adaptation of hepatocellular organelles to a longlasting hypothyroidism. Ten sham operated rats served as controls. All animals had free access to an Altromin-R standard diet and drinking water. The changes in hepatic cellular nuclei, organelles and membranes caused by thyroidectomy were examined. While scarcely any tetraploid nuclei could be found in the animals after 3 wk of hypothyroidism the degree of polyploidy increased strongly in the animals after 6 mo. of hypothyroidism, though it didn't reach that of the controls. After 6 mo. of hypothyroidism the chondrioma increased to twice its former volume. In contrast the mitochondria volume showed a considerable decrease after 3 wks of hypothyroidism. This mitochondrial hyperplasia is discussed as a false adaptation. It is the morphometric correlate of a cytoplasmic adaptation to an impaired mitochondrial function and cellular respiration. The equilibrium between the total substance of the chondrioma and the total cytoplasmic mass is disturbed in hepatocytes exposed to a 6 mo. hypothyroidism. The cristael membranes and the peroxisomes showed an inverse change of their morphometric values compared with the chondrioma. The chondrioma showed a hyperplasia, the cristael membranes and peroxisomes a hypoplasia. The population of peroxysomes after a consisted mainly mega-peroxysomes. This fact as well as the volumetric loss of the RER [rough endoplasmic reticulum] and the reduction of its membranes is to be seen as a consequence of the significantly impaired protein machinery after a long lasting hypothyroidism.

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