Freshwater zebrafish and brackish water rainbow trout were exposed to different concentrations of cadmium for up to 6 weeks. The gill morphology was examined by light and electron microscopy, and a morphometric analysis was performed. The morphometric study of the secondary lamellae revealed an increase in the portion exterior to the basal lamina, resulting in an increased diffusion distance, after exposure to cadmium concentrations of IOpgl-' and above. In both species this was due to an increase in volume of the non-tissue spaces of the secondary lamellar epithelium. Furthermore, the water space between neighbouring secondary lamellae was clearly reduced. Morphological examination revealed some gross alterations compared with control fish. These initially consisted in curling of the secondary lamellae and finally resulted in local teleangiectasia. Partial lifting of the secondary lamellar epithelium from the pillar cells resulted in large non-tissue spaces which were invaded by leucocytes. The first sign of degeneration was observed in the chloride cells, which were characterized by a dispersed cytoplasm and a smooth apical plasma membrane.

No abstract

Brown trout, Salmo trutta L., from two fish farms, situated within acid-susceptible areas in Sweden, were studied with respect to aluminium accumulation and gill pathology. The total aluminium concentrations, after liming of the water in both farms, were between 200 and 300//g/l at sampling. Brown trout from a third farm in a non-acidified area (total aluminium concentration of water 35/ig/l) were included as a control. The aluminium concentrations in gills from farmed brown trout in acidified areas were approximately 20/yg/g and 90//g/g wet weight respectively compared with approximately 2//g/g wet weight in control brown trout gills. Light-and electron microscopic examination disclosed two major types of gill lesions characterized by chloride cell hyperplasia in the secondary lamellar epithelium and enlargement of the intercellular spaces in the secondary lamellar epithelium. The difference in the aluminium speciation and accumulation may explain the difference in the gill pathology of farmed fish from acidified areas. The chloride cell hyperplasia together with a relatively low aluminium accumulation is considered to reflect a long-term exposure effect.

Brown trout gills were examined after exposure to different aluminium concentrations (50, 200, 500//g/l) at pH 5-5 and 7-0 for up to 6 weeks. The influence of humus (Pt 0, Pt 20) and water temperature (2-5X, 15X) was recorded. The gill structure was studied hy light, scanning and transmission microscopy, together with a complementary morphometric analysis of centrally located secondary lamellae. Low water temperature (2-5X) resulted in advanced gill lesions after exposure to aluminium at pH5-5. The lesionswerecharacterizedby enlargement of the secondary lamellae due to an increased number of chloride cells in the epithelia. Furthermore, the chloride cells contained cytoplasmic aluminium precipitates. Addition of humus (Pt 20) or increased pH (7 0) reduced or inhibited the effects of aluminium on the gills. A high water temperature (15''C) reduced the early gill lesions observed after exposure to water at 2-5°C. Prolonged exposure to a temperature of 15°C resulted in alterations in the gill structure in all groups, including the control group.