TCDD-induced alterations in gene expression profiles of the developing mouse paw do not influence morphological differentiation of this potential target tissue.

The aryl-hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that mediates the toxicity of certain halogenated aromatic hydrocarbons including 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD). These compounds are potent developmental toxicants that can alter gene expression and disrupt processes of proliferation and differentiation. It has not yet been determined which tissues during development are most sensitive to these compounds, nor which genes are directly associated with the toxicities.

Disruption of glomerular cell-cell and cell-matrix interactions in hydrocarbon nephropathy.

Environmental chemicals play an etiological role in greater than 50% of idiopathic glomerular diseases. The present studies were conducted to define mechanisms of renal cell-specific hydrocarbon injury. Female rats were given 10 mg/kg benzo(a)pyrene (BaP) once a week for 16 wk.

Characterization of glomerular cell phenotypes following repeated cycles of benzo[a]pyrene injury in vitro.

Exposure of cultured glomeruli to benzo[a]pyrene (BaP), a carcinogenic hydrocarbon, modulates mesangial and visceral epithelial cell proliferation in vivo and in vitro. The present studies were conducted to characterize mitogenic signaling profiles of cultured glomeruli following repeated cycles of BaP challenge. Enhanced rates of DNA synthesis were observed by the third passage in randomly cycling cultures after single or repeated carcinogen exposure.