During the study of five cases of acute yellow liver atrophy (which was reported in a previous paper), the author noted steatosis of the hepatic cell nuclei in all of the cases. In these cases there appeared a nuclear fat which showed neither a chromatin shell nor a clearly defined pale halo. The fats first appeared as fine granules but later they grow larger and glue together, forming irregular drops situated between the chromatin granules. This intranuclear fat is to be seen mostly in cases in which fatty degeneration of the hepatic cell is somewhat marked but degeneration of the nucleus is slight, and should be called a fatty degeneration as differing from physiological steatosis.
Studies were made on the steatosis of the hepatic cell nuclei in frogs (in summer) in which phosphorus was given causing experimental poisoning. A relatively large degree of steatosis was already noted on thethird day, and after the fifth day, a severe degree of steatosis was caused. Roughly parallel to the accumulation of fat in the protoplasma, fat appears in the nuclei in which degeneration is relatively slight.
The large perfectly round globules of fat inside the nuclei are almost always degeneration of the nucleoli, and on careful observation, recidua of the chromation shell could be seen around the droplets of fat. As the size of the fat dropletes increases, it deviates until its shell adheses to the inside of the nuclear membrane, and consequentely, a rupture of the nuclear membrane occurs there. On the occasion of there beging two nucleoli in a nucleus, there never occurs a simultaineous of the basic substance of the nucleus is intense, that of the nucleoli almost neyer occurs, and vice versa. Fat of the nucleus compared with that of the protoplasm, is more brilliant in its glimmer, sharper in its outline and, when stained with Sudan III, takes a more intense shade of red. These fats in the nucleus are mostly neutral fats.
After 11 to 14 days degeneration is intense in the cell body and nucleus, and when this is on the verge of necrosis, fat in the nucleus is completely absent. Therefore this intranuclear fat cannot be that of fat-phanerosis, but rather a product appearing in the nucleus through a pathological mechanism, and should belong to the category of fatty degeneration. Regenerated liver cells have little tendency to steatosis and nuclear fat does not appear.
The same experiment was made on frogs during their winter slumber, but no remarkable changes were found. This is probably due to the fact that the function of resorption of the intestines are at a very low level at this time.
Next, the liver cells were observed on the same material as mentioned above, after fixation by Professor Hamazaki's method using a mixture of sublimate and chrome and staining with carbolfuchsisn-odine. On summer frogs that had been given phosphorus for 3 to 6 days an increase in the K. E. S. was noted, inboth the protoplasm and the nucleus. The K. E. S. in the nucleus appeared diffusely or as minute granulae.
Comparing this with the results stained with Sudan III, the appearance of the K. E. S. approximately coincides with the appearance of neutral fats although in each case from the point of distribution and quantity they do not coincide, i.g. in phosphorus poisoned liver cells the increased K. E. S. has no direct relation with the metabolism disorder of the neutralfats.
In frogs during their winter slumber, increase of K. E. S. was not noted.
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