Elevated ammonia release from dystrophic chicken muscle cell and fibroblast cultures

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Abstract
The activity of adenosine monophosphate (AMP)‐aminohydrolase, the major NH3‐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 NH3 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 NH3 release, cells were incubated with 100 μg/ml of the protease inhibitor, leupeptin. Leupeptin reduced the rate of NH3 release by only 18.8% in normal muscle cells and 16% in dystrophic muscle cells. The release of NH3 was also higher from dystrophic chicken fibroblast cultures.