THE ACUTE TOXICITY AND HISTOPATHOLOGY OF BROOK TROUT (SALVELINUS FONTINALIS, MITCHILL) EXPOSED TO ALUMINUM IN ACID WATER

Fingerling brook trout were exposed to different concentrations of Al at pH 5.6. The Basic Static Acute Toxicity Test was used to determine the 96-hr. The toxicity of Al varied inversely with water hardness. The 96-hr LC(,50) at a hardness of 2, 18, and 40 mg/l (CaCO(,3)) was 0.37, 3.4, and 6.53 mg/l Al respectively. Darkening of skin color was possible due to an increase in Na ions in the water as a result of body ion loss, activating the hormone MSH which causes melanin granules to spread within the melanocytes. The method for evaluating the histological damage to the gills was developed. Edema in the gill suggests impairment of cell membrane permeability. Hyperplasia, fusion of lamellae, and sloughing of the epithelial cells were observed. In severe cases, the cellular structure of the gill was lost. The skin lost form due to different types of cell damage, including cytolysis and pycnotis. Lateral line canal neuromasts and supporting cells shrank and died. The necrotic neuromasts sloughed into the canal. The necrotic supporting cells separated from the damaged connective tissue sheath. Muscle showed shrunken and ruptured myofibrils, while sarcolemma were still connected. In the most severe cases, muscle fibers detached from the myocommata. Erythrocytes lost their structure, clumped and collapsed. In the kidney, swelling, vacuolation, and karyolysis of tubular cells were seen. Vacuolation of parenchymal cells, pycnosis, karyolysis, and karyorhexis occurred in the liver. Histology of all tissues of surviving fish appeared normal 3 months after transfer to uncontaminated water. The lateral line canal was regenerated by the end of the second month of the recovery period. In conclusion, we found that histology was essential to the interpretation of the toxicological effects of Al. The mortality of brook trout was attributed to Al toxicity that increased cell membrane permeability and mucification. Increased permeability resulted in the loss of body salt and an influx of Al and H ions. Mucus on gill surfaces caused anoxia leading to cell degeneration. Death was due to disturbances in osmoregulation, breakdown in enzyme activity, and disruption of O(,2) transport