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Impairment of Sodium Pump and Na⁺/H⁺ Antiport in Erythrocytes Isolated from Cancer Patients

Biophysics Laboratory, Faculty of Pharmacy, Université d'Aix-Marseille II [A. L. B., P. M. G., H. N. K., A. D. C.], and Oncology Unit, University Hospital Timone [A. E. N., R. G. F.], 13385 Marseille Cedex 5, France

We sought to determine whether the impairment of sodium pump activity and Na⁺/H⁺ exchange reported in tumorigenic cells was specific to these cells or more general. Sodium pump activity and Na⁺/H⁺ exchange were measured in erythrocytes from 49 cancer patients and 51 healthy subjects. Cancer patients with a newly detected cancer or in relapse and without associated pathologies known to modify these sodium transporters were included in this study.

Two sodium pump statuses reflecting its physiological modulation were evidenced for healthy subjects (10.3 ± 0.2 and 19.4 ± 0.8 mW/liter of cells). In cancer patients, only one basal status lower than those of controls was observed (8.3 ± 0.5 mW/liter of cells; P < 0.001). Cooperativity of the Na⁺/H⁺ antiporter is the same in cancer patients and controls (2.58 ± 0.27 versus 2.60 ± 0.15). The intracellular pH (pH_i) dependence curve of the antiporter was shifted toward more acidic values, and optimal pH_i was lower in cancer patients than in controls (5.80 ± 0.03 versus 6.08 ± 0.02; P < 0.0001). The mean maximal rate and the K_m of H⁺ for the Na⁺/H⁺ antiporter were higher: 8.4 ± 1.2 versus 4.6 ± 0.4 mmol H⁺/liter of cells/h (P < 0.01) and 514 ± 12 versus 322 ± 16 nM (P < 0.05), respectively.

Alterations of these Na⁺ transporters, therefore, were not restricted to cancerous cells. Among the alterations, the acidic shift in the pH_i dependence of Na⁺/H⁺ exchange appears associated with cancer because this behavior has never been reported in other pathologies.

¹ To whom requests for reprints should be addressed, at Laboratoire de Biophysique, Faculté de Pharmacie, Université D'Aix-Marseille II, 27 Boulevard Jean Moulin, 13385 Marseille Cedex 5, France. Phone: (33) 91-79-21-11; Fax: (33)91-80-26-12.

Received 7/18/95. Accepted 11/28/95.