2,3,7,8-Tetrachlorodibenzo-p-dioxin (
TCDD) has adverse effects on the development and function of the heart in zebrafish eleutheroembryos (embryos and larvae). We previously reported that
TCDD reduced blood flow in the mesencephalic vein of zebrafish eleutheroembryos long before inducing pericardial
edema. In the present study, we compared early
edema (pre-
cardiac edema), reduction of deduced cardiac output and reduction of blood flow in the dorsal aorta and cardinal vein caused by
TCDD. In the same group of eleutheroembryos,
TCDD (1.0 ppb) caused pre-
cardiac edema and circulation failure at the cardinal vein in the central trunk region with the similar time courses from 42 to 54 h post fertilization (hpf), while the same concentration of
TCDD did not significantly affect aortic circulation in the central trunk region or cardiac output. The dependence of pre-
cardiac edema on
TCDD concentration (0-2.0 ppb) at 55 hpf correlated well with the dependence of blood flow through the cardinal vein on
TCDD concentration. Several treatments that markedly inhibited
TCDD-induced pre-
cardiac edema such as knockdown of
aryl hydrocarbon receptor nuclear translocator-1 (ARNT1) and treatment with
ascorbic acid, an
antioxidant, did not significantly prevent the reduction of cardiac output at 55 hpf caused by 2.0 ppb
TCDD.
TCDD caused
hemorrhage and extravasation of
Evans blue that was intravascularly injected with
bovine serum albumin, suggesting an increase in endothelium permeability to
serum protein induced by
TCDD. The results suggest that the blood vessels are primary targets of
TCDD in
edema formation in larval zebrafish.