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.