Aims: Exudation of organic acid anions is one of the mechanisms responsible for aluminum (Al) tolerance. The plasma membrane (PM) H super(+)-ATPase is involved in the exudation of organic acid anions. However, the relationship between organic acid exudation and PMH super(+)-ATPase under Al toxicity remains unclear. This study aims to investigate the correlation among Al-induced citrate exudation, PMH super(+)-ATPase activity and counterions for citrate release from cluster roots of phosphorus-deficient (-P) white lupin. Methods: Al and various pharmacological agents were applied to incubate the cluster roots of P-deficient white lupin; the citrate exudation rate, PMH super(+)-ATPase activity and ion exudation of cluster roots were examined. Results: Citrate exudation from cluster roots of P-deficient white lupin was induced by 50 mu M Al treatment within 1.5 h, but no extra increase was found when the duration of Al treatment increased. The PMH super(+)-ATPase activity of cluster roots was insensitive to Al treatment, irrespective of Al concentration and duration of Al treatment. Al treatment increased K super(+) efflux but not H super(+) efflux from cluster roots. After application of pharmacological agents to P-deficient cluster roots under Al treatment or not, vanadate decreased H super(+) efflux and increased K super(+) efflux, but had no inhibitory effect on citrate exudation; fusicoccin increased H super(+) efflux and citrate exudation, but decreased K super(+) efflux; tetraethylammonium (TEA) chloride, a K super(+)-channel inhibitor, inhibited K super(+) efflux and increased H super(+) efflux. Conclusions: These results indicate that citrate exudation induced by combined treatment with P-deficiency and Al is independent of PMH super(+)-ATPase activity, and is coupled with K super(+) efflux, which may compensate H super(+) efflux for keeping the charge balance for Al-induced citrate exudation from cluster roots of P-deficient white lupin.