Aluminium toxicity to rainbow trout at low pH

An acute toxicity study of aluminium at low pH, using one-year-old rainbow trout (Salmo gairdneri R.), was performed in a closed recirculating system at pH 5.2, 5.4, and 5.6 with nominal concentrations of 0, 100, 200, and 400/tg A1/I. Mortality (96 h) was dependent on the pH and aluminium concentration. Measurements of aluminium in the plasma of exposed fish, by electrothermal atomic absorption spectrometry (ETAAS), showed a dose-dependent uptake of aluminium, but no correlation of plasma aluminium concentration to the mortality observed. Three major mechanisms of pH-A 1 toxicity seemed to prevail: i. Relatively low nominal aluminium concentrations (100 and 200 pg/1) at pH 5.2 as well as 200/tg AI/1 at pH 5.4 led to electrolyte loss possibly due to an interaction of aluminium with enzymes and epithelial tight junctions in the gill of the exposed fish. ii. Exposing fish to A1 concentrations ~ 100 ltg/1 and pH values //> 5.2 enhanced cell necrosis, proliferations, and fusions of the secondary lamellae in the gills resulting in the obstruction of the interlamellar space and thus most likely in the impairment of gas exchange. Aluminium fractionation suggested that inorganic monomeric A 1 was responsible for this tissue damage. iii. High aluminium concentrations ( ~ 200/tg/1) at moderately low pH (//> 5.4) led to clogging of the gills with mucus and thus to an impairment of gas exchange. This mucification was thought to stem from the physical irritation of the gills by accumulating polymeric A I.