Editing Ammonia (section)

=== Physiology ===
Ammonia plays a role in both normal and abnormal animal [[physiology]]. It is [[biosynthesis]]ed through normal amino acid metabolism and is toxic in high concentrations. The [[liver]] converts ammonia to [[urea]] through a series of reactions known as the [[urea cycle]]. Liver dysfunction, such as that seen in [[cirrhosis]], may lead to elevated amounts of ammonia in the blood ([[hyperammonemia]]). Likewise, defects in the enzymes responsible for the urea cycle, such as [[ornithine transcarbamylase]], lead to [[hyperammonemia]]. Hyperammonemia contributes to the confusion and [[coma]] of [[hepatic encephalopathy]], as well as the neurological disease common in people with urea cycle defects and [[organic aciduria]]s.<ref>{{cite book|author1=Zschocke, Johannes |author2=Hoffman, Georg |title=Vademecum Metabolism|publisher= Schattauer Verlag|year= 2004|isbn=978-3794523856}}</ref>

Ammonia is important for normal animal acid/base balance. After formation of ammonium from [[glutamine]], [[α-ketoglutarate]] may be degraded to produce two [[bicarbonate]] ions, which are then available as buffers for dietary acids. Ammonium is excreted in the urine, resulting in net acid loss. Ammonia may itself diffuse across the [[Nephron|renal tubules]], combine with a hydrogen ion, and thus allow for further acid [[excretion]].<ref>{{cite book|author1=Rose, Burton|author2=Helmut Rennke|title=Renal Pathophysiology|location=Baltimore|publisher=Williams & Wilkins|year=1994|isbn=978-0-683-07354-6|url=https://archive.org/details/renalpathophysio0000rose}}</ref>