RENAL FIBROSIS INDUCED BY IN UTERO AND LACTATIONAL EXPOSURE TO 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN IN RHESUS MONKEYS

fibrosis in marmosets by short range exposure 1 . In fibrotic myocardium, it was confirmed that proliferated components were not only collagen, but also fibronectin and laminin. Furthermore, TCDD induces endometriosis in the female monkey at a daily dose of 0.15 ng/kg/day for 4 years 2 . The effects of TCDD on proliferation of the extracellular matrix are possibly related to the increasing activation of growth factors such as TGF-β1and its receptor 1 . On the other hand, effects of TCDD on proliferation of the interstitial tissues of the offspring have not been well confirmed. It has been reported that TCDD alters extracellular matrix development in the kidney in the mouse fetus, when TCDD was administered to the pregnant mother 3 . In this report, however, decreasing of components of the extracellular matrix, such as fibronectin and collagen type IV, was described. It was concluded that the decreasing of the extracellular matrix results ultrastructural maldevelopments of the kidney. Recently, we observed renal dysgenesis in two postnatally dead young from mothers exposed to TCDD during the pregnancy and lactational period. In these two cases, renal corpuscles were mostly hypoplastic, and the interstitial tissues seem proliferated. These two cases were obtained by exposure to a high TCDD level, and these young died at the age of 406 days and 422 days. In the present study, we report that these two cases had renal fibrosis induced by TCDD exposure during the pregnancy and lactation, and show collagen proliferation in the kidney with picrosirius red staining.