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Elevated ammonia release from dystrophic chicken muscle cell and fibroblast cultures
Author(s) -
Young Ronald B.,
Hopkins Linda H.,
Fleming George D.
Publication year - 1984
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880070805
Subject(s) - fibroblast , ammonia , cell culture , neuromuscular junction , muscular dystrophy , chemistry , biology , medicine , endocrinology , microbiology and biotechnology , anatomy , genetics , biochemistry , neuroscience
The activity of adenosine monophosphate (AMP)‐aminohydrolase, the major NH 3 ‐producing enzyme in skeletal muscle, was approximately 35% lower in 7‐day dystrophic muscle cell cultures than in normal muscle cells cultures. However, the release rate of NH 3 from dystrophic muscle cells was 45% higher than that from normal muscle cells. The reasons for this apparent discrepancy are not clear. To determine indirectly if deamination of amino acids from protein degradation contributed to NH 3 release, cells were incubated with 100 μg/ml of the protease inhibitor, leupeptin. Leupeptin reduced the rate of NH 3 release by only 18.8% in normal muscle cells and 16% in dystrophic muscle cells. The release of NH 3 was also higher from dystrophic chicken fibroblast cultures.

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