S-adenosyl- l-methionine, related compounds, and cerebral enzymatic activities during chronic hyperammonemia in rats

The effect of the im administration of some chemicals in the S-adenosyl- l-methionine system on the hyperammonemia syndrome was evaluated. This experimental syndrome was induced in the rat by ip administration of high doses of ammonium acetate (33, 100, and 300 mg/kg/day, 6 days a week for 40 days, followed by study of the activity of some cerebral enzymes involved in energy transduction. The enzymatic activities evaluated in the homogenate and/or in the mitochondrial fraction of brain tissue were: lactate dehydrogenase, citrate synthase, malate dehydrogenase, total NADH-cytochrome c reductase, and cytochrome oxidase. The lowest and highest doses of ammonium acetate did not induce any significant change in cerebral enzymatic activities, while the median dose reduced the activity of malate dehydrogenase (in the homogenate) and of total NADH-cytochrome c reductase (both in the homogenate and in the mitochondrial fraction). The simultaneous daily im treatment with equimolar doses of substances involved in the S-adenosyl- l-methionine system (adenosine, methionine, and S-adenosyl- l-methionine) did not cause any significant modification of the cerebral enzymatic activities associated with the administration of ammonium acetate at the three dose levels.