Some aspects of ammonia toxicity on the gill pathology of carp (Cyprinus carpio L.) and trout (Salmo gairdneri R.)

Abstract

The toxic effects of ammonia on the gill structure of common carp, Cvprinus carpio L. and rainbow trout Salmo gairdneri R., were investigated by both light microscopic histological studies, scanning and transmission electron microscopical studies. Experimental procedures adopted included the use of standard dilution water under constant temperature conditions and commonly used buffers to stabilize the pH, while additional experiments were also conducted in non buffered dilution water. The common pathological changes noted for both carp and trout included severe chloride cell proliferation, excessive mucous secretions and an infiltration of large numbers of eosinophilic granular cells into the gill epithelia. Prolonged exposure to high concentrations of ammonia resulted in progressive necrosis of chloride, mucous and eosinophilic granular cells. Apoptotic changes indicative of cell death in the gill epithelium included the appearance of condensed darkened cells, and cells with nuclear changes such as pyknosis and karyorrhexis. Dilation of mitochondria, loss of mitochondrial matrix, and appearance of dark inclusions were particularly noted in the carp gill chloride cells. Damage to the mucous cells consisted of premature occlusion of the mucous vesicles and flocculation of the mucous material within the mucous cells, resulting in progressive vacuolations, necrosis and thus a reduction in the stainable population of mucous cells. However, specific lesion types varied between the carp and trout. Carp gills developed massive hyperplastic and hypertrophic lesions comprising of grossly swollen gill epithelial and infiltration cells under buffered experimental conditions, while such lesions were not only less extensive in non buffered experimental conditions but the tissue changes were dominated by the loosening and sloughing of the gill epithelium. Discrepancies in the histological alterations were however evident as a consequence of the presence of buffers and hence the very validity of the recommendation and use of buffer chemicals in toxicity testing was questioned. In the case of trout no hyperplastic lesions such as those seen in carp were not seen but an increased inter and intra cellular oedema was characteristic. Under normal water hardness conditions trout gills apparently showed no variations due to the presence of different buffers or in the non-buffered water conditions. But under high hardness conditions and in the presence of buffer, the gill, lesions were more extensive and necrotic. The results suggest that while ammonia brings about necrotic changes in the gill tissues of both, carp and trout, the lesions arc more necrotic in carp than in trout. These results also indicate that the indiscriminate use of buffers and variations in the water quality conditions might have been the cause of wide variations in the reported toxicity values of ammonia to fish in addition to the reported differences in pathology in the available published literature. The recent reports of a small number of workers that ammonia per se does not cause any pathology is not supported by the present investigations.