2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos.
2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos.
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2,3,7,8-四氯二苯并-p-二恶英在发育中的异斜眼底胚胎中诱导细胞凋亡和细胞色素 P4501A 表达。
DOI:
10.1016/s0166-445x(00)00161-2
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发表时间:
2001
期刊:
影响因子:
--
通讯作者:
DiGiulio,RT
中科院分区:
文献类型:
--
作者:
Toomey,BH;Bello,S;Hahn,ME;Cantrell,S;Wright,P;Tillitt,DE;DiGiulio,RT
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 LC50and LD50of 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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