alexa Cytopathology of liver and in rainbow trout Oncorhynchus mykiss after long-term exposure to sublethal concentrations of linuran


Toxicology: Open Access

Author(s): asmina Oulmil, Negele RD, Braunbeck T

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Hepatic and renal cytopathological alterations in fingerling rainbow trout Oncorhynchus mykiss following 5 wk exposure to 30, 120, and 240 mu g l(-1) linuron [3(3,4-dichlorophenyl)-1-methoxy-1-methylurea] were studied by electron microscopy. Ultrastructural alterations were detected in liver and kidney at greater than or equal to 30 mu g l(-1), 2 orders of magnitude below conventional LC(0). The response suggested a dose-response relationship with a change from adaptive to degenerative features al 120 mu g l(-1). Hepatocyte changes included: stimulation of mitosis; segmentation of nuclei; partial reorganization of heterochromatin; multiplication of nucleoli; fractionation, vesiculation and transformation of rough endoplasmic reticulum (RER) into myelinated bodies; induction of smooth endoplasmic reticulum; moderate steatosis; apparent proliferation of mitochondria, peroxisomes, Golgi fields and lysosomal elements; depletion of glycogen; perisinusoidal lipid accumulation; elevated rate of hepatocytes in various stages of necrosis; infiltration and increased phagocytic activity of macrophages. Reactions of renal tubular cells were differentiated in different nephron segments. Major alterations by site in kidney were (1) renal corpuscle: lobulation of podocyte nuclei; (2) proximal segment I: elevated heterogeneity of all cell components, increased heterochromatin and nuclear size, rearrangement of RER, proliferation of Golgi fields, novel lysosomal elements, decreased mitochondria and lysosomes at 240 mu g 1(-1); (3) proximal segment II: nuclear lobulation, binucleated cells, proliferation of lysosomes and peroxisomes (lower concentrations), decreased peroxisomes and mitochondria (240 g mu l(-1)), crystalline inclusions in lysosomal matrix, fragmentation, degranulation and circular arrangement of RER; (4) distal segment: induction of giant mitochondria with longitudinal crystalline inclusions, atypical lysosomes with long crystalline matrix inclusions, and augmentation of various lysosomal elements. Comparison of linuron-induced cellular alterations with cytopathological effects by potential linuron breakdown products, namely 4-chloroaniline and 3,4-dichloroaniline, revealed a high degree of similarity of cytopathological phenomena, indicating that part of the changes observed after linuron exposure might well be due to the action of linuron metabolites.

This article was published in Diseases of Aquatic Organisms and referenced in Toxicology: Open Access

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