Nitrogen Excretion And Defense Against Ammonia Toxicity

  • Chew S
  • Wilson J
  • Ip Y
 et al. 
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Abstract

Most tropical teleost fishes are ammonotelic, producing ammonia and excreting it by diffusion of NH3across the gills. Accumulation of ammonia in the body can be due to either the inability to excrete or convert nitrogenous wastes or to a net influx of NH3from the environment. Although all three conditions could lead to increases in ammonia levels in the tissues of the fish, it is important to differentiate the source of the ammonia being detoxified, which is often neglected in the literature. When confronted with alkaline pHenv, terrestrial conditions or low levels of environmental (exogenous) ammonia, fishes have difficulties in excreting ammonia that is endogenously produced (Figure 8.4, Table 8.1). Fishes, with few exceptions, are very susceptible to elevated tissue ammonia levels under adverse conditions. Some could, however, avoid endogenous ammonia toxicity by utilizing several physiological mechanisms, and consequently manifest high tolerance to aerial exposure. Suppression of proteolysis and/or amino acid catabolism may be a general mechanism adopted by some fishes during aerial exposure. Others, like the giant mudskipper, P. schlosseri, which uses amino acid as an energy source while active on land, reduces ammonia production by utilizing partial amino acid catabolism, leading to the accumulation of alanine. Some fishes convert excess endogenous ammonia to less toxic compounds, including glutamine and other amino acids for storage. A few species have active OUC and convert endogenous ammonia to urea for both storage and excretion. Under conditions of slightly elevated ambient ammonia, P. schlosseri can continue to excrete endogenous ammonia by active transport of ammonium ions. There are indications that some fishes can manipulate the pH of the body surface to facilitate NH3volatilization during aerial exposure or ammonia loading. In contrast, fishes have to detoxify not only endogenous ammonia, but also exogenous ammonia that has penetrated into the body when they are confronted with HEA which results in a reversed PNH3gradient (Figure 8.5, Table 8.1). To deal with exogenous ammonia, the most effective way is to manipulate the pHenvthrough increased CO2and acid (H+) excretion to lower the concentration of NH3in the external medium. This means NH3is, in effect, detoxified to NH4+externally, constituting a strategy of "environmental detoxification." Another way is to accumulate high levels of ammonia in the body, especially in the blood, to rebuild a more favorable PNH3to reduce the influx of exogenous ammonia, or even to regain ammonia excretion. When ammonia builds up internally, as long as it is below a critical level, the brain is protected by the detoxification of ammonia to glutamine. It has been suggested that some fishes would "fix" ammonia to free amino acids during ammonia loading. However, the simultaneous build-up of essential amino acids, although to a different extent, in all cases suggests a reduction in amino acid catabolism to reduce endogenous ammonia production instead. Furthermore, this strategy is usually auxiliary to the accumulation of ammonia in tissues and the blood. As an individual event, it does not seem appropriate to "fix" the penetrating exogenous ammonia because it would simply draw in exogenous ammonia continuously. The same argument would apply to urea formation, which is highly energy-dependent, in fish during severe ammonia loading. Some fishes (elasmobranchs, holocephans, and coelacanths) evolved to synthesize and accumulate urea as an osmotic component (ureosmotic). The utilization of urea, an end-product of nitrogen catabolism, for osmotic purposes has an energetic advantage - the energy derived from carbon catabolism of the amino acids is not lost. In order to be able to retain urea for osmoregulation, effective urea permeabilities would have to decrease, as seen in extant marine elasmobranchs through modifications of the lipid composition of gills, and re-absorption of urea by specific secondarily active (Na+-coupled) urea transporters in gills and kidney. However, for those elasmobranchs adapted secondarily back to a fresh- or brackish-water environment, there must be a reduction in the capacity of urea synthesis and/or the capacity of urea retention. © 2005 Elsevier Inc. All rights reserved.

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