Abstract

Summary In order to elucidate whether and when and age-dependant polyploidization process takes place in the course of normal growth of the organ, analogous to that in the myocardium, the DNA content was studied in 26 livers and in 24 hearts. Human material between the ages of the 28th week of gestation and the 17th year of life were employed. The organs were weighed and prepared within 60 hours after death. DNA content was determined in the hearts and livers using the diphenylamine reaction according to Dische and Burton. Feulgen cytophotometric measurements obtained the DNA content of individual cell nuclei and the various ploidy levels of the tissue. Using the quantitative relationship of connective tissue to parenchymal tissue nuclei obtained histologically and the corresponding organ weight, the absolute cell number in the organ was computed. These studies led to the following results: 1. The biochemically determined DNA concentration in the liver is more than 2.0 mg/g tissue and decreases to approximately 1.0 mg/g at birth, after which it remains at this level as a constant until the 17th year of life. 2. The total amount of DNA in the liver increases from 50 mg at the end of the fetal period to over 1500 mg at the age of 17 years. 3. Over 90% of the parenchymal cells in the liver are diploid until the 8th year of life, after which more than 10% tetraploid cells appear, whose proportion increases to at most 15% up to the 15th year of life. Higher ploidy level cells cannot be found in morphologically unremarkable organs. 4. The total cell count in the liver increases from 20 × 10 9 cells at birth to approximately 70 × 10 9 cells at 6 years old; at age 15 years 180 × 10 9 cells are present in the liver. Mesenchymal and parenchymal cells increase in parallel during this time. The number of parenchymal cells amounts to 10 × 10 9 at birth and 110 × 10 9 at the age of 15 years. Although functional loading appears to be involved as a stimulus for polyploidization in the heart, many observations point to the idea that the ploidy level in the liver is hormone-dependent. This idea is supported by our observations of a case of adrenal cortical atrophy with ploidy level in the hepatocytes which was elevated above normal.

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