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2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and
cytochrome P4501A expression in developing Fundulus heteroclitus
embryos.
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 LC(50) and LD(50) of TCDD
for Fundulus embryos were approximately 19.7+/-9.5 pg TCDD/microl
(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. PMID:
11311389