Cellular distribution and induction of CYP1A following exposure of gilthead seabream, Sparus aurata, to waterborne and dietary benzo(a)pyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin: an immunohistochemical approach.

The present study aimed to investigate cellular expression of cytochrome P4501A (CYP1A) protein in the seabream, Sparus aurata, exposed to one of two CYP1A-inducing contaminants, benzo(a)pyrene (B(a)P) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Male adult fish were exposed to several concentrations of TCDD or B(a)P either via water or via food. Fish were sampled after 0, 5, 10, 15 or 20 days of treatment and the time- and concentration-dependent induction of CYP1A protein in cells and tissues was studied using immunohistochemistry. A general site of CYP1A induction was the vascular endothelium. Aqueous exposures resulted in elevation of CYP1A immunoreactivity in gill pillar cells, heart endothelium, renal tubular epithelium, hepatocytes, and gut mucosal epithelium. In contrast, dietary exposure resulted in strong CYP1A immunostaining in gut epithelium but in only mild to moderate staining elsewhere. Both B(a)P and TCDD induced CYP1A in similar cellular response patterns in most organs examined, although TCDD generally led to higher staining intensity and frequency (i.e. the number of CYP1A-positive cells within an organ), an effect that is likely to be related to compound-specific differences in induction potency, metabolism and penetration. Contaminant-specific staining patterns were observed in the gills, where TCDD exposure evoked CYP1A immunostaining in the endothelial pillar cells, while B(a)P induced CYP1A staining in the branchial epithelial cells. This work points to the importance of immunohistochemical identification of cell-specific CYP1A responses in assessing the toxicology of CYP1A-inducing xenobiotics.