2,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos
Identifieur interne : 000394 ( Istex/Curation ); précédent : 000393; suivant : 0003952,3,7,8-Tetrachlorodibenzo- p -dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos
Auteurs : Barbara Holland Toomey [États-Unis] ; Susan Bello [États-Unis] ; Mark E. Hahn [États-Unis] ; Susannah Cantrell [États-Unis] ; Peggy Wright [États-Unis] ; Donald E. Tillitt [États-Unis] ; Richard T. Di Giulio [États-Unis]Source :
- Aquatic Toxicology [ 0166-445X ] ; 2000.
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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.
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DOI: 10.1016/S0166-445X(00)00161-2
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Barbara Holland Toomey<affiliation><mods:affiliation>Corresponding author. Present address: 411 Millbrook Road, Middletown, CT 06457-5543, USA. Tel.: +1-860-3449634</mods:affiliation><wicri:noCountry code="subField">449634</wicri:noCountry></affiliation><affiliation><mods:affiliation>E-mail: btoomey@dellnet.com</mods:affiliation><wicri:noCountry code="no comma">E-mail: btoomey@dellnet.com</wicri:noCountry></affiliation><affiliation><mods:affiliation>E-mail: btoomey@dellnet.com</mods:affiliation><wicri:noCountry code="no comma">E-mail: btoomey@dellnet.com</wicri:noCountry></affiliation><affiliation><mods:affiliation>1 Also corresponding author. Tel.: +1-919-6138024; fax: +1-919-6848741.</mods:affiliation><wicri:noCountry code="no comma">1 Also corresponding author. Tel.: +1-919-6138024; fax: +1-919-6848741.</wicri:noCountry></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: richd@acpub.duke.edu</mods:affiliation><country wicri:rule="url">États-Unis</country></affiliation>Le document en format XML
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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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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