Location: Aquatic Animal Health Research
Title: Susceptibility of channel catfish (Ictalurus punctatus) fed dietary sodium chloride to nitrite toxicity Authors
Submitted to: Aquaculture Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: December 1, 2006
Publication Date: February 26, 2007
Citation: Welker, T.L., Lim, C.E., Aksoy, M., Klesius, P.H. 2007. Susceptibility of channel catfish (Ictalurus punctatus) fed dietary sodium chloride to nitrite toxicity. Aquaculture Conference Proceedings. Aquaculture 2007. February 26 - March 2, 2007 San Antonio , Texas. p. 990. Technical Abstract: Toxicity of nitrite to fish is caused by the oxidation of hemoglobin (Hb) to form methemoglobin (MetHb), which is incapable of binding oxygen. Methemoglobinemia causes blood to turn brown in color and has been termed “brown blood disease”. Treatment of nitrite toxicity in fish has primarily consisted of increasing the water chloride concentration through addition of sodium chloride (NaCl) or calcium chloride (CaCl2) to ponds. The protective effect of chloride against MetHb formation has been attributed to competitive inhibition of nitrite uptake by chloride cells at the gills. Supplementation of fish diets with NaCl has shown promise in preventing toxicity to water-born cations, such as copper in rainbow trout, by elevating sodium levels in blood. However, the effect of dietary NaCl in prevention of toxicity of fish to water-born anions, such as nitrite, has not been studied. Juvenile channel catfish (Ictalurus punctatus) were fed nutritionally complete, practical basal diets supplemented with NaCl at 0, 1, 2, or 4 % of diet to apparent satiation twice daily for 10 weeks. Catfish were exposed to nitrite after six (7.70 mg/l nitrite-N) and ten (7.18 mg/l nitrite-N) weeks of feeding to determine the effect of dietary NaCl supplementation on resistance to nitrite toxicity. Fish were sampled before (baseline, pre-exposure) and after 24 h nitrite exposure to determine the effects of dietary NaCl on hematology (hematocrit, Hb, and MetHb) and plasma electrolyte dynamics (nitrite, chloride, sodium, and potassium). Mortality from nitrite toxicity was also determined. Mortality from nitrite exposure decreased with increasing NaCl in diet at 6 weeks and was significantly lower in the 4% NaCl group (12.5%) than in the control group (57.5%). Although a similar trend in mortality occurred at 10 weeks, the differences among dietary treatments were not significant. A direct link between the effect of dietary NaCl supplementation on measured physiological parameters, such as MetHb or plasma nitrite levels, and mortality from nitrite exposure could not be established. Even though plasma chloride was generally higher in NaCl-fed fish, the increases were not significant, but the therapeutic effect of dietary NaCl may have been supplemental to other detoxification mechanisms not measured. It is possible that supplementation of diets with NaCl may have provided better protection against methemoglobinemia in channel catfish at lower nitrite exposure concentrations or at some time prior to 24 h, the endpoint used in the exposure tests. The acute levels of nitrite used in this study resulted in MetHb levels that were approximately 90% or greater, which is considerably higher than the levels (is greater than or equal to 50% MetHb) deemed detrimental to fish health, and the effects of dietary salt supplementation on lower levels of nitrite toxicity should be explored in the future.