The urea cycle converts nitrogen from amino acid degradation into urea using enzymes. The enzyme argininosuccinase catalyzes the breakdown of argininosuccinate to produce the amino acid arginine, which reacts with water to form urea. However, a deficiency in argininosuccinase results in argininosuccinate excretion and hyperammonemia. How would you treat argininosuccinase deficiency?

Arginase Deficiency

Explanation:

Arginase deficiency is an acquired issue that causes the amino acid arginine (a structure square of proteins) and ammonia to collect gradually in the blood High protein meals or stress brought about by sickness or periods without food (fasting) may make ammonia amass all the more rapidly in the blood Argininosuccinic aciduria is an uncommon hereditary issue described by deficiency or absence of the chemical argininosuccinate lyase (ASL) The absence of this argininosuccinate lyase in over the top aggregation of nitrogen, as smelling salts (hyperammonemia), in the blood