Ammonia production, excretion, toxicity, and defense in fish: a review

Abstract

Many fishes are ammonotelic but some species can detoxify ammonia to glutamine or urea. Certain fish species can accumulate high levels of ammonia in the brain or defense against ammonia toxicity by enhancing the effectiveness of ammonia excretion through active NH4+transport, manipulation of ambient pH, or reduction in ammonia permeability through the branchial and cutaneous epithelia. Recent reports on ammonia toxicity in mammalian brain reveal the importance of permeation of ammonia through the blood–brain barrier and passages of ammonia and water through transporters in the plasmalemma of brain cells. Additionally, brain ammonia toxicity could be related to the passage of glutamine through the mitochondrial membranes into the mitochondrial matrix. On the other hand, recent reports on ammonia excretion in fish confirm the involvement of Rhesus glycoproteins in the branchial and cutaneous epithelia. Therefore, this review focuses on both the earlier literature and the up-to-date information on the problems and mechanisms concerning the permeation of ammonia, as NH3, NH4+ or proton-neutral nitrogenous compounds, across mitochondrial membranes, the blood–brain barrier, the plasmalemma of neurons, and the branchial and cutaneous epithelia of fish. It also addresses how certain fishes with high ammonia tolerance defend against ammonia toxicity through the regulation of the permeation of ammonia and related nitrogenous compounds through various types of membranes. It is hoped that this review would revive the interests in investigations on the passage of ammonia through the mitochondrial membranes and the blood–brain barrier of ammonotelic fishes and fishes with high brain ammonia tolerance, respectively.

Net ion fluxes and ammonia excretion during transport of Rhamdia quelen juveniles

“…This situation cause stress, which increases cortisol levels in silver catfish (BARCELLOS et al, 2001;2004) and stimulates glycogenesis, gluconeogenesis, protein catabolism and ammonia production (RANDALL & TSUI, 2002;IP & CHEW, 2010). Silver catfish net Na + , K + and Cl -effluxes through the transport increased with the increase of loading density, demonstrating that high loading density increases ionoregulatory stress in this species.…”

“…The high transport cost request the use of a small amount of water and the highest load density possible, which cause accumulation of metabolites and deteriorate water quality (GOLOMBIESKI et al, 2003). Ammonia is the dominant end product of nitrogen metabolism in most teleosts, including silver catfish (GOLOMBIESKI et al, 2013), and is toxic at low concentrations (IP & CHEW, 2010). During transport the concentration of this metabolite increases and may be a potential risk that influences fish survival and duration of transport (GOMES et al, 1999;GOLOMBIESKI et al, 2003;CARNEIRO et al, 2009).…”

Role of Bioflavonoid Quercetin on Expression of Urea Cycle Enzymes, Astrocytic and Inflammatory Markers in Hyperammonemic Rats

“…Ammonia is formed in mammals by the catabolism of proteins and other nitrogenous compounds; at elevated levels ammonia is toxic, causing dysfunction of cerebral activity [1][2][3]. Under normal conditions, a major portion of ammonia is released into portal circulation and is detoxified in liver.…”

Toxicidade aguda da amônia em juvenis de sardinha-verdadeira Sardinella brasiliensis

“…Ammonia is the main nitrogenous excrement of teleost fish and is produced from the catabolism of dietary protein (EDDY, 2005;IP and CHEW, 2010). In the aqueous solution, ammonia exists in two forms: un-ionized ammonia (NH3-N) and ionized ammonium (NH4+-N), and their sum composes the total ammonia nitrogen (TAN).…”

“…Ammonia is excreted through the gill epithelium either by passive diffusion as NH3-N along a gas partial pressure gradient between fish blood and water, or through active transport as NH4+-N in exchange for sodium (HARGREAVES andKUCUK, 2001, BARBIERI, 2010). The NH3-N/NH4+-N equilibrium is determined by pH and temperature (IP and CHEW, 2010).…”