Abstract

Pathogenesis of indium-caused tail malformations was investigated by in vivo and in vitro experiments. In the in vivo experiment, pregnant Wistar rats received single intravenous administration of indium trichloride at 0.4 mg/kg on day 10 of gestation, and their embryos were examined on days 11, 12 and 13. Embryos in the indium group showed caudal hypoplasia from day 11. Increased apoptosis was observed in their tailbud on day 11. Similar effects were observed in the in vitro experiment, when day 10 rat embryos were cultured in the presence of indium trichloride at 50 μM for 24 h and for further 24 h in the absence of indium. It was considered from these results that caudal hypoplasia probably due to excessive cell loss by increased apoptosis in the tailbud accounted for indium-caused tail malformations in rat fetuses, and that indium-caused embryotoxic effects were direct effects on the conceptus.

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