Effect of lanthanum on red blood cell deformability


Alexy T., Nemeth N., Wenby R. B., Bauersachs R. M., Baskurt O. K., Meiselman H. J.

BIORHEOLOGY, cilt.44, sa.5-6, ss.361-373, 2007 (SCI-Expanded)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 44 Sayı: 5-6
  • Basım Tarihi: 2007
  • Dergi Adı: BIORHEOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.361-373
  • Anahtar Kelimeler: deformability, electrophoresis, lanthanum, red blood cell, membrane, HUMAN-ERYTHROCYTE-MEMBRANE, VISCOELASTIC PROPERTIES, NEURAMINIDASE, PERMEABILITY, TRANSPORT, PROTEINS, RIGIDITY, FUSION, IONS, FLOW
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Prior reports describing the effects of lanthanum (La3+) on red blood cells (RBC) have focused on the effects of this lanthanide on cell fusion or on membrane characteristics (e. g., ion movement across membrane, membrane protein aggregation); the present study explores its rheological and biophysical effects. Normal human RBC were exposed to La3+ levels up to 200 mu M then tested for: (1) cellular deformability using a laser-based ektacytometer and an optical-based rheoscope; (2) membrane viscoelastic behavior via micropipettes; (3) surface charge via micro electrophoresis. La3+ concentrations of 12.5 to 200 mu M caused dose-dependent decreases of deformability that were greatest at low stresses: these rheological changes were completely reversible upon removing La3+ from the media either by washing with La3+-free buffer or by suspending La3+-exposed cells in La3+-free media (i.e., viscous dextran solution). Both membrane shear elastic modulus and membrane surface viscosity were increased by 25-30% at 100 or 200 mu M. As expected, La3+ decreased RBC electrophoretic mobility (EPM), with EPM inversely but not linearly associated with deformability; changes of EPM were also completely reversible. These results thus indicate novel aspects of RBC cellular and membrane rheological behavior yet raise questions regarding specific mechanisms responsible for La3+-induced alterations.