Objective   To deter mine whether Cd affect E-cadherin-dependent adhesion junctions in the proximal tubule cells in vivo.

  Methods   Two groups of rats were used for the study.Animals in the Cd-treated group were given subcutaneous injection of CdCl ₂(containing Cd 1.4 mg/kg, 3 days per week for up to 4 weeks).A nimals in the control group received injections of the saline alone at the same time.After 4 weeks, 24 h urine samples were collected.Renal cortex was as glutathione(GSH)and malondialdehyde(MDA)contents in renal cortex.General kideney morphology and expression of E-cadherin were mensur ated.

  Results   Urinary LDH activities as well as protein contents in the Cd-treated group increased significantly compared with those in the control group.The slight increase of GSH contents in renal cortex was significant.There was no significant change in MDA contents in renal cortex.The proximal tubule cells in the samples from the Cd-treated animals showed avery ragged, and massive brush border appeared to falling off, with partia vacuolede naturalization.E-cadherin was less present in the basolateral surface in the samples from the Cd-treated animals than from the control animals.

  Conclusion   Cd can disrupt E-cadherin-dependent adhesion junctions in the proximal tubule in vivo, which is the presence of a low level of oxidative stress.E-cadherin may be the relatively early target of nephrotoxic actions of Cd.And the damage of E-cadherin-mediated adhesion may contribute to nephro to xicity of Cd.