Dioxin-induced up-regulation of the active form of vitamin D is the main cause for its inhibitory action on osteoblast activities, leading to developmental bone toxicity.

Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is known to cause bone toxicity, particularly during animal development, although its action mechanism to cause this toxicity has yet to be elucidated. Mouse pups were exposed to TCDD via dam's milk that were administered orally with 15 microg TCDD/kg b.w.

Critical role of cyclooxygenase-2 activation in pathogenesis of hydronephrosis caused by lactational exposure of mice to dioxin.

Congenital hydronephrosis is a serious disease occurring among infants and children. Besides the intrinsic genetic factors, in utero exposure to a xenobiotic, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has been suggested to induce hydronephrosis in rodents owing to anatomical obstruction in the ureter. Here, we report that hydronephrosis induced in mouse pups exposed lactationally to TCDD is not associated with anatomical obstruction, but with abnormal alterations in the subepithelial mesenchyma of the ureter.

Localization of cytochrome P450 1A1 in a specific region of hydronephrotic kidney of rat neonates lactationally exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Hydronephrosis is typically observed in terata caused by in utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), via the arylhydrocarbon receptor, but the molecular mechanism underlying its pathogenesis is largely unknown. In the present study, pregnant Holtzman rats were treated once by gavage with TCDD (1.0 microg/kg bw) or corn oil on gestation day 15.

Disruption of thyroid hormone homeostasis at weaning of Holtzman rats by lactational but not in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The purpose of this study is to clarify whether lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is entirely responsible for the perturbation in thyroid hormone homeostasis during the neonatal period. Pregnant Holtzman rats were given a single oral dose of 1.0 mug TCDD/kg body weight on gestational day 15.