Nitrite (NO2) is an intermediate step in nitrification of ammonias (NH4+ and NH3) to nitrate (NO3). In aquacultural waters nitrite forms primarily as a byproduct of microbial metabolism, and to a much lesser extent, by chemical oxidation/reduction reactions. In the presence of oxygen, certain types of aerobic bacteria (Nitrosomonas spp.) are able to derive energy from the oxidation of ammonia to nitrite. Also, when anaerobic conditions prevail, some types of heterotrophic bacteria are able to utilize nitrate as a terminal electron receptor in energy metabolism. Nitrate is reduced with the formation of nitrite. The rate is slow for this reaction. Nevertheless, both nitrification and denitrification can contribute to nitrite level in fish culture ponds. Denitrification only occurs in bottom sediments or in areas devoid of oxygen. Nitrite is apparently not directly assimilated by aquatic plants as a source of nitrogen for protein synthesis.
Nitrite may build-up in tilapia culture ponds or tanks due to any of the following conditions:
When chloride level is low in the culture water, nitrite in modest concentrations (low parts per million) is toxic to tilapia and other fish. In alkaline water nitrite is actively transported from the water into the blood by the same mechanism in gill chloride cells that transports chloride. The chloride pump moves nitrite into the blood over a concentration gradient. Nitrite and chloride compete for the same transport receptor sites on the gill chloride cells. The rate of nitrite uptake is modified by the availability of chloride in the water.
However, pH of the water can influence nitrite diffusion across the gills. If the pH is very low (e.g. < 6) much of the nitrite in water is in the form of nitrous acid (HNO2). Nitrous acid diffuses rapidly across gill epithelium and is unaffected by the presence of chloride. Thus, low pH conditions coupled with elevated nitrite can result in methemoglobinemia in the blood of tilapia even in the presence of high chloride in the water.
The principal mechanism of nitrite toxicity is the binding to hemoglobin to form methemoglobin, a reversible form of hemoglobin that does not bind or transport oxygen. Methemoglobin changes the color of the blood from the normal red to muddy-red or brown. This color change can be detected on gross inspection of the gills. Since methemoglobin does not transport oxygen, asphyxiation is the principal reason fish die from nitrite poisoning.
It follows that toxicity effects are more likely from nitrite exposure when dissolved oxygen level is low. In addition, exposure to sublethal nitrite level has been found to decrease the resistance of channel catfish to bacterial infection.
Because of there is competitive interaction between chloride and nitrite for the same receptors, water of even low salinity (e.g. ~ 1 part per thousand) should provide sufficient chloride to protect tilapia from lethal nitrite poisoning. In addition, sodium chloride can be added to water ( 1 gram per liter) to protect tilapia in freshwater from the effects of high nitrite. Further information about use of chloride to treat nitrite toxicity is given in the Treatment Module (in the section on use of salt).
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