Abstract

The effect of indium on gap junctional communication was investigated in primary cultured rat hepatocytes. Treatment of hepatocytes with indium chloride at concentrations of 100 μM to 1 mM for 2 h resulted in dose-dependent inhibition of gap junctional communication between hepatocytes. The effect of indium on hepatocytes was also evaluated using two indices for cell viability: lactate dehydrogenase (LDH) leakage and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction. Indium did not cause any increase in LDH leakage from hepatocytes at the above concentrations, but inhibition of MTT reduction was observed at concentrations above 500 μM. These results suggest that the gap junctions between hepatocytes may be vulnerable sites to indium toxicity.

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