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Am J Physiol Renal Physiol 275: F143-F153, 1998;
0363-6127/98 $5.00
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Vol. 275, Issue 1, F143-F153, July 1998

Cadmium is more toxic to LLC-PK1 cells than to MDCK cells acting on the cadherin-catenin complex

L. B. Zimmerhackl, F. Momm, G. Wiegele, and M. Brandis

Department of Pediatrics, Albert-Ludwigs-University, D-79106 Freiburg, Germany

Cadmium toxicity to renal cells was investigated in Madin-Darby canine kidney (MDCK) and LLC-PK1 cells as models of the distal tubule/collecting duct and proximal tubule, respectively. Cells were grown on two-compartment filters and exposed to 0.1-50 µM Cd2+. In MDCK cells, Cd2+ was more toxic from the basolateral than from the apical side and dependent on the extracellular Ca2+ concentration. Toxicity was evident within 24 h, as shown by a decrease in transepithelial resistance (TER), reduced proliferation (bromodeoxyuridine incorporation), reduction in ATP concentration, and morphological changes. On confocal microscopy, E-cadherin and alpha -catenin staining patterns indicated interference with the cadherin-catenin complex. LLC-PK1 cells showed a similar toxicity pattern, which was evident at lower Cd2+ concentrations. An increase of E-cadherin and alpha -catenin molecules in the Triton X-100-insoluble fraction was detectable at high Cd2+ concentrations in LLC-PK1 cells but not in MDCK cells. Lactate dehydrogenase release indicated membrane leakage in LLC-PK1 cells. Rhodamine-phalloidin staining, a probe for F-actin filaments, demonstrated alterations of the actin cytoskeleton in both cell lines. In conclusion, cadmium caused ATP depletion and interfered with the cadherin-catenin complex and probably the tight junctions changing renal cell morphology and function.

cell proliferation; epithelial cell polarity; transepithelial resistance; adenosine 5'-triphosphate cytoskeleton


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