Anion-dependent transport of thallous ions through human erythrocyte membrane

Undirectional fluxes of 204Tl+ through the human red blood cell membrane were measured. The inward rate coefficient measured in a K(+)-free saline was 15.6 +/- 0.6 hr-1. The influx of Tl+ could be partially inhibited with 0.1 mM ouabain (by 28%), 0.1 mM DIDS (by 50%) or 1 mM furosemide (by 51%). The...

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Veröffentlicht in:The Journal of membrane biology 1992-12, Vol.130 (3), p.219-225
Hauptverfasser: Skulskii, I A, Gusev, G P, Sherstobitov, A O, Manninen, V
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Sprache:eng
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Zusammenfassung:Undirectional fluxes of 204Tl+ through the human red blood cell membrane were measured. The inward rate coefficient measured in a K(+)-free saline was 15.6 +/- 0.6 hr-1. The influx of Tl+ could be partially inhibited with 0.1 mM ouabain (by 28%), 0.1 mM DIDS (by 50%) or 1 mM furosemide (by 51%). The inhibitory effects of ouabain and DIDS or furosemide were additive. Half-maximal responses were seen at 0.72 microM and 0.22 mM concentrations of DIDS and furosemide, respectively. A similar action of these blockers on Tl+ influx was observed in the erythrocytes incubated in MgCl2-sucrose media. The outward rate coefficient of 204Tl was also inhibited by DIDS and furosemide (by 65 and 52%, respectively). Rate coefficients of 204Tl influx and efflux decreased significantly in the red cells exposed to Cl(-)-free media (NaNO3 or Mg(NO3)2-sucrose). Under these conditions addition of DIDS and furosemide led to only a small inhibition of Tl+ fluxes. There was a linear increase in Tl+ influx with rising of external Cl- concentration within 80-155 mM or HCO3- concentration from 20 to 40 mM when the sum of anions was kept constant (155 mM) with NO3-. The HCO3(-)-stimulated Tl+ influx was completely blocked by 0.05 mM DIDS but only 67% by 1 mM furosemide. The present study provides direct evidence for the occurrence of Cl- (HCO3-)-dependent, DIDS-sensitive movement of Tl+ across the human erythrocyte membrane in both directions. Under physiological conditions, about half of net Tl+ fluxes occurs due to an anion exchange mechanism.
ISSN:0022-2631
1432-1424
DOI:10.1007/BF00240479