An epithelial cell culture model for sturgeon integument responds sensitively to 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure.

Sturgeon species are threatened or endangered worldwide due to habitat loss and increasing pollution. An epithelial cell culture model promises to help investigate hazardous environmental exposures. Stratified squamous integument of green and white sturgeons (Acipenser medirostris and transmontanus, respectively) and cells cultured from their epithelia expressed substantial levels of TGM1-like transglutaminases, types I and II keratins and aryl hydrocarbon receptor (AHR) proteins analogous to those in mammalian integument. Epithelial cells cultured from the rim of the mouth, oral cavity and ampullae of Lorenzini exhibited dramatic growth suppression upon exposure to environmentally relevant levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a model compound for ubiquitous environmental combustion products that activate the AHR. The rho kinase inhibitor Y27632 markedly increased cell growth in culture and, surprisingly, prevented growth suppression by TCDD. Thus, these epithelial cell cultures provide an intriguing model for studying the mechanism by which activation of the AHR produces adverse effects. Evidently, contributions from genome duplication, gene duplication, gene loss and complications of polyploidization have endowed sturgeon with multiple forms of AHR, in this case 3 pairs of closely related genes. AHR1 and AHR2 are predicted to bind TCDD with high affinity, which could help rationalize the cellular sensitivity to AHR activation.