2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos

Authors

Barbara Holland Toomey, Duke UniversityFollow
Susan Bello, Woods Hole Oceanographic Institute
Mark E. Hahn, Woods Hole Oceanographic InstituteFollow
Susannah Cantrell, U.S. Geological Survey
Peggy Wright, U.S. Geological Survey
Donald E. Tillitt, U.S. Geological SurveyFollow
Richard T. Di Giulio, Duke UniversityFollow

Document Type

Article

Date of this Version

2001

Citation

Aquatic Toxicology 53 (2001) 127–138

Abstract

Fundulus heteroclitus embryos were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC₅₀ and LD₅₀ of TCDD for Fundulus embryos were ~19.7 ± 9.5 pg TCDD/µl (water bath) and 0.25 ± 0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction.