Phosphate absorption by Arabidopsis thaliana: interactions between phosphorus status and inhibition by arsenate.

The effects of phosphorus status and arsenate on the absorption of phosphate by roots of intact sterile seedlings of Arabidopsis thaliana were studied by analysing the rate of depletion of phosphate from solutions initially containing 10 M KH2PO4. Depletion of phosphate from the experimental solutions was measured both chemically and by labelling with 32P. There was a substantial efflux of phosphate coincident with a rapid influx of phosphate, with efflux increasing with increasing phosphorus status. The highest rates of absorption were obtained for the plants initially grown with a high level of phosphorus but then deprived of phosphate for 5 d prior to the experiments, with the next highest rates obtained for the most phosphorus-deficient plants. Kinetic analysis suggests that changes in both the affinity and capacity of the absorption mechanism contribute to differences in the rate of phosphate influx between plants of different phosphorus status. Arsenate as 20 M KH2AsO4 inhibited phosphate influx in a manner such that all plants, regardless of their phosphorus status, had the same phosphate influx rate. This was reflected in identical values for the Michaelis constant, Km, and maximum velocity as used in Michaelis–Menten kinetics, Vmax. Arsenate had its greatest effect on phosphate movement to the shoot. The simultaneous elimination of differences in phosphate influx between plants of different phosphorus status suggest that phosphate movement to the shoot may be important in the regulation of influx by phosphorus status.

Urea, Creatinine and Phosphate Kinetic Modeling during Dialysis: Application to Pediatric Hemodialysis

The kinetics of urea, creatinine and phosphate removal during dialysis were investigated in pediatric patients using a two-pool model taking into account fluid shifts and mass transfer between the two compartments. It is found that even urea must be described by a two-pool model since it presents a post dialysis rebound due to equilibration between the two compartments. Phosphate plasma concentration drops very sharply during the first hour of dialysis and rises rapidly during the rebound period. This pattern cannot be accounted for by the classical two-pool model with constant generation rate and mass transfer coefficients, but corresponds to a large time-dependent phosphate influx from the intracellular compartment in which phosphate is generated by biochemical reactions or liberated from the bones. This influx was calculated for four patients representing 8 dialysis sessions and was found to reach a plateau after 90 minutes of dialysis, dropping rapidly during the rebound period.

Phosphate transport in kidneys: effect of transmembrane electrical potential

The effect of a transmembrane electrical potential on phosphate transport by kidney brush-border membrane vesicles was studied. The initial rate of Na(+)-dependent phosphate influx was twice as high as that of efflux. Generation of a negative transmembrane potential had a stimulatory effect on the rate of influx but had no effect on efflux. The Na+ saturation curve for phosphate influx was sigmoidal, and the Hill coefficients were similar, in the presence and absence of a transmembrane potential. The membrane potential increased both the affinity for phosphate and the maximal velocity (Vmax) of the transporter. In the absence of a Na+ gradient, the stimulation by the potential was 1.78-fold. When a proton gradient (in greater than out) was the driving force, the electrical potential stimulated phosphate transport 1.71-fold. Internal Na+ (trans) inhibited phosphate influx whether a potential was present or not. Internal phosphate (trans) stimulated phosphate influx in the absence of a potential but not in its presence. These results indicate that the electrical potential is an important driving force for the Na(+)-phosphate carrier and that the translocation of the carrier is a potential-dependent step.