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  • Title: [The cellular mechanisms of the regeneration of the cirrhotic liver in rats. I. The correlation of the processes of cellular proliferation, polyploidization and hypertrophy after the cessation of chronic exposure to carbon tetrachloride].
    Author: Sakuta GA, Kudriavtsev BN.
    Journal: Tsitologiia; 1996; 38(11):1158-70. PubMed ID: 9082615.
    Abstract:
    Using cytofluorimetry and absorptive cytophotometry, DNA and total protein contents were measured in hepatocytes of intact rats (the initial weight 180-200 g), and of rats chronically poisoned with CCl4 for 6 months, and then 1, 3 and 6 months after the end of poisoning. It has been found that in the course of development of the cirrhotic liver damage, the protein content in hepatocytes and their ploidy level rise by 63 and 40%, respectively, compared to control animals of the same age. On termination of poisoning, the mean ploidy decreased but still exceeded the control level by 25% even after 6 months of recovery. This was due mainly to the higher, than in norm, number of mononuclear octaploid hepatocytes. The protein amount per diploid hepatocyte returned to the control level by the end of recovery. Special calculations have shown that during those 6 months, when the experimental animals were poisoned, the increase in the liver mass of control rats was due completely to the hepatocyte DNA syntheses, i.e. proliferation and polyploidization, making 69 and 31%, respectively. Within the next 6 months, polyploidization in the control rat liver fell down to zero, whereas the liver cell hypertrophy (i.e. the increase in cell cytoplasm) rose by 24%. Meanwhile the growth of the liver in the CCl4-poisoned rats was due to all the three processes: the hepatocyte proliferation, the increase in cell genome number (polyploidization), and hypertrophy of the hepatocyte cytoplasm making respectively, 50, 30 and 20%. The postcirrhosis recovery occurred almost completely at the expense of hepatocyte proliferation. The contribution of polyploidization to the recovery was, in fact, negative, because of depolyploidization of liver parenchyma cell population. The involvement of cell hypertrophy was first noticeable only by the end of recovery, when the liver growth regained features characteristic of the normal liver.
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