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Liver autophagy in the influenza B virus model of Reye's syndrome in mice

✍ Scribed by Beulah M. Woodfin; Larry E. Davis


Publisher
John Wiley and Sons
Year
1986
Tongue
English
Weight
286 KB
Volume
31
Category
Article
ISSN
0730-2312

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✦ Synopsis


Biochemical evidence is presented for the autophagic destruction of liver mitochondria in the influenza B virus model of Reye's syndrome in mice. Separation of lysosomes and autophagic vacuoles from mitochondria was accomplished by prior treatment of the mice with Triton WR-1339, resulting in uptake of detergent by these organelles (tritosomes), reducing their densities. The organelles were banded in a discontinuous sucrose gradient. Total protein in the heavy tritosomal fraction increased from 1-2% in controls to 7-8% in virus-treated animals. Omithine carbamoyl transferase (OCTase), a mitochondrial marker, increased from 2-3 % (controls) to 11-15 % (virus-treated), and glucose-6-phosphatase, a marker for endoplasmic reticulum, increased from 1-2% (controls) to 8-10% (virustreated). P-Galactosidase, a soluble enzyme in the lysosome, and OCTase also increase in the cell extract fraction following virus treatment, indicating that there was turnover of heavy lysosomal contents.


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