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Cadmium inhibits ABCG2 transporter function in BeWo choriocarcinoma cells and MCF-7 cells overexpressing ABCG2

M Kummu1, E Sieppi, K Wallin

  • 1Department of Pharmacology and Toxicology, Institute of Biomedicine, University of Oulu, P.O. Box 5000, 90014 Oulu, Finland.

Placenta
|August 16, 2012
PubMed

Insights

Cadmium, lead, and methylmercury are neurotoxic. While heavy metals did not alter placental ABCG2 transporter expression, cadmium chloride inhibited its function, potentially impacting fetal protection.

Area of Science:

  • Toxicology
  • Molecular Biology
  • Pharmacology

Background:

  • Heavy metals like cadmium, lead, and methylmercury pose neurotoxic risks to developing fetuses.
  • The ABCG2 transporter in the human placenta is crucial for protecting the fetus from xenobiotics by effluxing compounds into maternal circulation.

Purpose of the Study:

  • To investigate the impact of cadmium chloride, lead chloride, and methylmercury chloride on the expression and function of the ABCG2 transporter in human placental cells.
  • To determine if these heavy metals affect the transport activity of ABCG2.

Main Methods:

  • Human placental BeWo choriocarcinoma cells were used to assess ABCG2 expression via immunoblotting and RT-PCR.
  • ABCG2 function was evaluated by measuring the efflux of substrates like mitoxantrone and (14)C-PhIP.
  • Cytotoxicity of heavy metal compounds was determined using MTT assays.

Main Results:

  • All tested heavy metal compounds (CdCl2, PbCl2, MeHgCl) exhibited cytotoxicity, with MeHgCl being the most potent.
  • Cadmium chloride (CdCl2) significantly inhibited the efflux of ABCG2 substrates, indicating impaired transporter function.
  • Heavy metals did not affect the protein or mRNA expression levels of ABCG2, nor the mRNA of ABCC1 or ABCC2.

Conclusions:

  • Cadmium chloride impairs the function of the placental ABCG2 transporter, despite not affecting its expression.
  • Further research is needed to ascertain if this functional inhibition leads to increased placental transfer of ABCG2 substrates to the fetus.
  • The findings highlight a specific mechanism by which cadmium may pose a risk to fetal development via placental transport disruption.

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