Abstract
The mechanisms operating for the maintenance of an optimal adenine nucleotide pool in tissues are interrelated with the metabolism of AMP. This compound is the parent adenine nucleotide molecule to be produced, either de novo from nonpurine molecules, or by salvage from preformed purines. At the same time it is also the substrate for adenine nucleotide degradation to diffusable nucleosides and bases, which can efflux from the tissue. The present study was undertaken to clarify the mechanisms operating in the skeletal and heart muscles to produce and degrade AMP. Primary rat myotube and cardiomyocyte cultures were utilized as models. The activity of the various pathways was gauged in intact cells, under physiological conditions, employing labeled precursors. In addition some of the key enzymes were assayed in cell extracts.
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