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Cadmium-induced apoptosis in rat kidney epithelial cells involves decrease in nuclear factor-kappa B activity.

Jianxun Xie1, Zahir A Shaikh

  • 1Department of Biomedical and Pharmaceutical Sciences and Center for Molecular Toxicology, College of Pharmacy, University of Rhode Island, Kingston, Rhode Island 02881, USA.

Toxicological Sciences : an Official Journal of the Society of Toxicology
|February 16, 2006
PubMed
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Cadmium exposure triggers apoptosis in kidney cells by suppressing nuclear factor-kappa B (NF-kappaB) activity, potentially through oxidative stress. Restoring NF-kappaB function protects cells from this damage.

Area of Science:

  • Toxicology
  • Cell Biology
  • Molecular Biology

Background:

  • Renal epithelial cells undergo apoptosis when exposed to toxic substances like cadmium (Cd).
  • Nuclear factor-kappa B (NF-kappaB) is a transcription factor known to regulate genes involved in apoptosis.
  • Understanding the role of NF-kappaB in cadmium-induced apoptosis is crucial for cellular protection strategies.

Purpose of the Study:

  • To investigate the involvement of the NF-kappaB transcription factor in cadmium-induced apoptosis of rat kidney proximal tubular epithelial cells (NRK-52E).
  • To elucidate the mechanisms by which cadmium affects NF-kappaB activity and its downstream targets.
  • To determine if oxidative stress mediates the suppression of NF-kappaB by cadmium.

Main Methods:

  • NRK-52E cells were exposed to varying concentrations of cadmium chloride (CdCl2).

Related Experiment Videos

  • NF-kappaB DNA-binding activity, IkappaB kinase alpha activity, and protein phosphorylation (IkappaB-alpha, NF-kappaB p65) were assessed.
  • Apoptosis was quantified using flow cytometry, and caspase activation and DNA fragmentation were measured.
  • Cells were pretreated with antioxidants or NF-kappaB inhibitors/activators to evaluate their effects.

    • Main Results:

    • Cadmium exposure decreased NF-kappaB DNA-binding activity and inhibited IkappaB kinase alpha in a dose- and time-dependent manner.
    • Cadmium reduced the phosphorylation of IkappaB-alpha and NF-kappaB p65, and decreased levels of NF-kappaB target genes (cIAP-1, cIAP-2).
    • Cadmium induced caspase activation, DNA fragmentation, and apoptosis, which were attenuated by antioxidants and NF-kappaB activation, but potentiated by NF-kappaB inhibition.

    Conclusions:

    • Cadmium-induced apoptosis in renal epithelial cells involves the suppression of NF-kappaB activity.
    • Oxidative stress may play a role in mediating the inhibitory effects of cadmium on NF-kappaB.
    • Modulating NF-kappaB activity offers a potential therapeutic strategy against cadmium-induced kidney injury.