Abstract

Elevated concentrations of nitrite and/or nitrate are a potential problem in aquatic ecosystems. Freshwater crayfish, Astacus astacus, were exposed to 1 mM nitrite or 1 mM nitrate in order to study uptake and physiological effects of these ions. Additionally, recovery from nitrite intoxication was investigated. Crayfish exposed to 1 mM ambient nitrite accumulated nitrite in the haemolymph to a concentration of 17.6 mM within 7 days. Haemolymph [NO 3 −] increased in parallel to 25.4 mM. The nitrate was endogenously produced, suggesting that more than half the nitrite taken up was detoxified by endogenous conversion to nitrate. Nitrite uptake induced a 40% reduction in both haemolymph [Cl −] and haemolymph [Br −], supporting the view that Cl −, Br − and NO 2 − compete for the same uptake mechanism (i.e. the active branchial Cl − uptake mechanism). Haemolymph sulphate and phosphate concentrations were not significantly affected by nitrite exposure. The extracellular amino acid concentration increased while the extracellular osmolality decreased, suggesting a volume-induced release of cellular amino acids to the extracellular compartment. Nitrite was completely eliminated from the haemolymph when nitrite-exposed crayfish were returned to nitrite-free water for 7 days. Concomitantly, extracellular [Cl −] and osmolality recovered to control values. Haemolymph [NO 3 −], however, remained significantly elevated, revealing a slow elimination of nitrate. In control animals, nitrate was passively distributed between haemolymph and water. Nitrate uptake was minor in crayfish exposed to 1 mM ambient nitrate. One week of nitrate exposure was not sufficient to reach a new equilibrium distribution, revealing a low branchial permeability to nitrate.

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