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Ultrastructural Changes of Liver Cell Mitochondria in Autolysis.
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Original Article Ultrastructural Changes of Liver Cell Mitochondria in Autolysis.
Yoon Kyung Sohn, Il Hoon Kwon, Tae Joong Sohn
Journal of Pathology and Translational Medicine 1985;19(3):290-301
DOI: https://doi.org/
Department of Pathology, Kyungpook National University, Taegu, Korea.
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The authors studied the ultrastructural changes of liver cell mitochondria in autolysis. The male Sprague-Dawley rats, weighting 140~160 gm were sacrificed for extract liver tissue. The slices of the liver tissue were incubated in 37 degrees C aseptic normal saline, and those were examined by following intervals; 10, 20 and 30 minutes and 1, 2, 6, 12 and 24 hours with light and electron microscope. The results obtained by light microscopy were summerized as follow. Several fine intracytoplasmic vacuoles were observed 1 hour after incubation. After 3 hours, focal destruction of cytoplasmic membrane with pyknosis of nuclei were observed. More delicate intracytoplasmic architectural changes could not be detected at light microscopic studies. The cord arrangement and cellular boundaries were relatively well preserved until 24 hours after incubation. Electronmicroscopically, mild intramitochondrial swelling with diminution of intramatrical granules were observed at 20 minutes. These were the earliest findings. Both high amplitude swelling and destruction of mitochondrial membrane were observed concurrently at 1 hour after incubation. The earlier membrane changes were observed at inner membrane with cristae and followed by degeneration of the outer membrane. The intramatrical amorphous dense deposits were observed at 30 minutes when the membranes were not destroyed. These deposits were noted in the other experimental groups which were incubated longer than 30 minutes. More electron dense deposits were observed after 1 hour at that time the membrane changes appeared. Vhe results suggest in this experiment that the earliest autolytic changes of liver cell mitochondria is loss of intramitochondrial granules and the membraneous changes led to the irreversible mitochondiral injury. The appearance of two types of intramitochondrial dense deposits would be an interesting finding needed to require further investigation for the chemical stucture and mechanism of dense deposit formation.

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