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Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
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Bisphenol A differently inhibits CaV3.1, Ca V3.2 and Ca V3.3 calcium channels

Pavlovičová Michaela1, Karmažínová Mária, Huláková Silvia

  • 1Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Vlárska 5, 833 34, Bratislava, Slovak Republic.

Naunyn-Schmiedeberg'S Archives of Pharmacology
|October 31, 2013
PubMed

Insights

Bisphenol A (BPA) affects T-type calcium channels, crucial for heart and brain function. Even at low, environmentally relevant concentrations, BPA impacts these channels, potentially explaining health issues linked to this common contaminant.

Area of Science:

  • Biochemistry
  • Toxicology
  • Neuroscience

Background:

  • Bisphenol A (BPA) is a ubiquitous environmental contaminant found in most of the US population.
  • Epidemiological studies link BPA exposure to cardiovascular and neuronal disorders.
  • BPA is known to interact with hormone receptors and voltage-dependent ion channels.

Purpose of the Study:

  • To investigate the effects of Bisphenol A (BPA) on T-type calcium channels.
  • To determine the concentration-dependent mechanisms of BPA's action on these channels.

Main Methods:

  • Utilized whole-cell patch clamp technique to measure calcium currents.
  • Expressed recombinant T-type calcium channel subtypes (CaV3.1, CaV3.2, CaV3.3) in HEK 293 cells.
  • Analyzed concentration-dependent effects of BPA on channel activity, gating, and kinetics.

Main Results:

  • BPA inhibited T-type calcium channel currents in a concentration-dependent manner.
  • Nanomolar BPA concentrations preferentially inhibited CaV3.2 and CaV3.1 subtypes without altering gating kinetics.
  • Micromolar BPA concentrations accelerated current decay, shifted inactivation voltage dependence, and reduced current amplitudes, suggesting pore blockage at high concentrations.

Conclusions:

  • BPA modulates T-type calcium channel gating and can physically obstruct the channel pore at higher concentrations.
  • Observed effects occur within the range of BPA concentrations found in human biological fluids.
  • These findings suggest a potential mechanism for BPA's contribution to cardiovascular and neuronal health issues.

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