Hepatocellular dysfunction results in impaired clearance of ammonium by the liver.
Urea has low toxicity even at high concentration, in contrast to its precursors, particularly ammonia.
Glutamine synthesis is altered under several pathological conditions.
Synaptically released glutamate is removed by uptake into the surrounding astrocytes and it is cycled via the glutamine-glutamate-cycle.
The glutamate-nitricoxide-cGMP pathway modulates some forms of learning and memory. Additional feasible mechanism for impaired energy metabolism in hepatic encephalopathy (HE) and hyperammonemia is the mitochondrial permeability transition (mPT).