Ecotoxicological assessment of water quality and ecosystem health: a case study of the Volga river / Moiseenko T. I., Gashkina N. A., Sharova Yu. N., Kudryavtseva L. P. // Ecotoxicology and Environmental Safety. - 2008. - Т. 71, № 3. - С. 837-850.

844 T.I. Moiseenko et al. / Ecotoxicology and Environmental Safety 72 (2008) 837-850 5. Fish pathology Various deviations from the physiological norm were found in all the fish of investigated river sections. 5.2. Gills In some cases, the gills were pale (their normal color is scarlet) with a clearly distinct anemic ring along the gill arc. The largest number of fish with an anemic ring was caught in the Gorkii Reservoir and in the Lower Volga (downstream of Astrakhan). Epithelium desquamation in secondary lamellae (Fig. 3c), swelling of the distal parts of filaments, and shortening, curvature, and fusion of secondary lamellae (Fig. 3b) were observed, which resulted in the transformation of the rigidly structured gill into an unstructured mass, with the distal filament alone still functioning. Congestive phenomena (stasis) were found in most of the respiratory lamellae, which is related to the violation of capillary conductivity. Vast hemorrhages were observed between filaments and secondary lamellae (Fig. 3d). In certain filaments, the secondary lamellae were completely destroyed. Extensive 1am- melar hypertrophy with some proliferation from the bases of the secondary lamellae was recorded. 5.2. Liver Changes in the liver color, dimensions, and texture were observed. All the bream caught in different river sections had increased loose-textured liver with color varying from a mosaic light-brown to pale yellow. In some cases, the liver was liquified; it had clearly distinct parts of necrosis or pronounced signs of atrophy. All the examined fish demonstrated signs of liver disease of differing degrees of severity. Frequent visible disturbances of this organ were typical of fish caught in the Gorkii (up to 92.6% of a the fish) and Kuibyshev (up to 54.5% of the fish) reservoirs, as well as in certain sections of the Lower Volga (Table 4). Morphological and functional changes in the liver manifested themselves in the form of lipoid dystrophy (Fig. 4b) and hydropic dystrophy (Fig. 4c), which are symptoms of progressive hepato- pathy. In the case of intensified intoxication, lipid and hydropic dystrophy of hepatocytes were often found. Hydropic dystrophy is a variation of protein dystrophy and is related to the disturbance of protein and water exchange. In this case, the permeability of cell membranes increases, vacuoles appear in the cytoplasm due to water ingress, the cellular organelles are destroyed, while the cell itself becomes filled with water and dies. In the case of lipoid dystrophy, fat occlusions, which almost completely fill the cells, appear in the hepatocytes. Diffuse disruptions of bream liver, accompanied by disturbances in the morphological structure of liver lobules and pronounced necrosis of liver tissue, were also diagnosed. Mechanisms of lipoid and protein dystrophy development are similar. Frequently, they develop under the conditions of the organism intoxication or accompany hypoxia. In some micro­ scopic sections, complete necrosis (not that of a “ hotbed” character) of the liver tissue was observed (Fig. 4d). Interstitial proliferative inflammation related to hepatocyte necrosis and the appearance of inflammation infiltrates were also diagnosed. In the process of their development, the cells of the infiltrates transform into collagenous fibres of connective tissue. As a result, a thick connective-tissue capsule can appear around the zone of necrosis. Such progressive necrosis and structural reorganization of the tissue can contribute to post-necrotic hepatic cirrhosis, leading, in turn, to hepatic failure. Vast zones of parenchymal hemorrhage, destruction of blood corpuscles and blood vessel walls, as well as proliferation of connective tissue around the blood vessels, were revealed. Signs of chronic congestive hyperemia in liver veins were found. They testify to varicose veins and capillaries, a decrease in b Fig. 3. Pathological changes in the gills of bream (arrowed): a—normal structure (F —filament, L—lamellae), x 160; b—extensive lamellar hyperplasia with fusion of secondary lamellae, x 320; с—separation of epidermis at base of secondary lamellae, x 320; and d—hemorrhage, x 160.

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