The interaction of chloride with the sulfate transport system of ehrlich ascites tumor cells

✍ Scribed by Charles Levinson

• Publisher: John Wiley and Sons
• Year: 1976
• Tongue: English
• Weight: 630 KB
• Volume: 87
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1040870212

✦ Synopsis

The effect of C1-on S 0 4 -2 efflux was studied in both C1-containing and C1--free ascites tumor cells loaded with 3 5 S 0 4 -2 to test the hypothesis that C1 --S04-2 exchange is mediated by the same mechanism responsible for S04-2-self exchange.

The addition of C1--free, 3 5 S 0 4 -2 loaded cells to a S04-2-free, C1-medium results in: (1) S04-2 efflux that is dependent on the extracellular C1-concentration (Km = 4.85 mM; k e = 0.048 min-1 at 50 mM Cl-) and ( 2) net C1-uptake that exceeds SO4 -2 loss. Both SITS (4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate) and ANS (I-anilino-8-napthalene sulfonate) inhibit S 0 4 -2 efflux but are without effect on C1-uptake.

The addition of C1--containing, 3 5 S 0 4 -2 loaded cells to a SO,-Wree, C1-medium results in: (1) a slight gain in cellular C1-and (2) k efor S 0 4 -2 efflux identical to that for C1--free cells.

The results are compatible with the suggestion that: (1) C1-interacts with a membrane component responsible for transmembrane SO4 -2 movement; (2) C1-interaction stimulates the rate of unidirectional S04-2 efflux from cells initially free of C1-as well as the rate of S04-2 turnover in cells maintained in the steady state with respect to C1-and S04-2; and (3) in the case of cells initially free of C1-, the C1--S04-2 pathway represents only a small fraction of the total unidirectional C1--influx the remainder being compatible with the electroneutral accumulation of NaCl and KCl.