Histopathological alterations and induction of cytochrome P-450 1A in the liver and gills of the gilthead seabream (Sparus aurata) exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Abstract

The toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been demonstrated in the seabream Sparus aurata specimens. Liver presented hepatocytic alterations, with an increase of lipid droplets and glycogen granules. Ultrastructural modifications of hepatocytes included RER fractionation, glycogen augmentation, as well as a rise in the number of lipid droplets, vacuoles and secondary lysosomes. In the gills, secondary lamellar epithelium showed hyperplasia, hypertrophy and lamellar fusion on the edge of the filaments. At the end of the exposure period (1 pg1(-1) TCDD for 20 days), some organelles in epithelial cells of the secondary lamellae and the tubular system of the chloride cells appeared altered. In the liver of TCDD-exposed specimens, immunoreactive cytochrome P-450 1A was concentrated close to the cytoplasmic and nuclear membranes, and positive granules were also evident throughout cytoplasm of the hepatocytes. Significant cytochrome P-450 staining was especially evident in endothelium of the hepatic vascular system. At the beginning of the exposure (1 pg 1(-1) TCDD, for 5 and 10 days), cytochrome P-450 immunostaining was observed in the cytoplasm of scarce hepatic cells and after 20 days of treatment, specific immunostained cytoplasmic granules were detected in most hepatocytes. In gills of TCDD-treated specimens, pillar-endothelial cells showed a cytochrome P-450 1A immunostaining concentrated close to the base of gill filaments and dispersed through the gill lamellae. There was also significant cytochrome staining of the endothelium of the branchial vascular system. However, no cytochrome immunoreactivity was observed in epithelial-respiratory cells.