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

Abstract

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 (HNO 2 ) 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.