Uptake and loss of nitrite from the blood of rainbow trout, Salmo gairdneri Richardson, and Atlantic salmon, Salmo salar L. in fresh water and in dilute sea water

The acute toxicity of nitrite (NO−2) to salmonids is strongly ameliorated by chloride (Cl−) ions rendering it almost harmless in most fresh waters apart from those with low Cl− content. In Cl− poor fresh water external NO−2 is concentrated in the blood plasma until it is at approximately the same molar concentration as haemoglobin (about 8 mmol) and at this point most of the haemoglobin has been oxidized to methaemoglobin this being a contributory cause of death. Two theories are advanced to account for NO−2 concentration in the blood. The first supposes that gills are impermeable to NO−2 but allow its conjugate acid nitrous acid (HNO2) to diffuse into the blood where it dissociates according to the blood pH value. Thus NO−2 will accumulate in the blood plasma if it has a higher pH value than the water. The second supposes that the Cl− uptake mechanism in the freshwater gill has an affinity for NO−2 and accounts for the fact that NO−2 entry to the blood is suppressed when external Cl− is present in significant amounts. The results also suggest that NO−2 and Cl− behave similarly as diffusing ions. Thus NO−2 diffusion into the blood of seawater fish and from the blood of NO−2 loaded freshwater fish occurs at approximately the same rate as the corresponding Cl− fluxes. Nitrite loss from seawater fish is thought to be mainly by diffusion although there is some evidence for the active Cl− extrusion mechanism having a weak affinity for nitrite.