Chloride-Stimulated sulfate efflux in Ehrlich ascites tumor cells: Evidence for 1:1 coupling

✍ Scribed by Mitchel L. Villereal; Charles Levinson

• Publisher: John Wiley and Sons
• Year: 1977
• Tongue: English
• Weight: 679 KB
• Volume: 90
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1040900317

✦ Synopsis

The kinetics of C1--S0,-2 exchange in Ehrlich ascites tumor cells was investigated in an attempt to determine the stoichiometry of this process.

medium are placed in SO,+-free, 25 mM C1-medium, both the net amount and rate of C1-uptake far exceeds SO,-2 loss. Addition of the anion transport inhibitor SITS (4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid) greatly reduces sulfate efflux (97%), but has no measurable effect on chloride uptake. Addition of furosemide, a C1-transport inhibitor, reduces chloride uptake 94% but is without effect on sulfate efflux. These findings suggest that a chloride permeability pathway exists distinct from that utilized by SO,-2.

SITS, when added to furosemide treated cells, further reduces chloride uptake as well as inhibiting sulfate efflux, and under these experimental conditions, a linear relationship exists between SITS-sensitive, net chloride uptake and sulfate loss. The slope of this line is 1.05 (correlation coefficient = 0.996) which suggests the stoichiometry of Cl--SO,-* exchange is 1:l. Assuming a 1:1 stoichiometry, measurement of the initial chloride influx and initial sulfate efflux indicate that 92% of net chloride uptake is independent of sulfate efflux.

Taken altogether, these results support the contention that the tumor cell possesses a permeability pathway which facilitates the exchange of one sulfate for one chloride. Under conditions where anion transport is not inhibited, this coupling is obscured by a second and quantitatively more important pathway for chloride uptake. This pathway is SITS-insensitive, although partially inhibited by furosemide.