Galactose uptake by human platelets in vitro

Galactose transport by human platelets has been studied by measuring the cellular accumulation of the radiolabeled sugar during brief periods of suspension in varying concentrations of galactose. Weighted least-squares regression curves fitted to the measurements (initial velocity versus galactose concentration) indicate that a kinetic model with two saturable components is statistically more consistent with the data than a model based upon a single process ($\text{P < 0.001}$). For the two-component model $\text{K}{}_{\mathrm{<mtext>m</mtext><mtext>1</mtext>}}\text{= 0.29}$ mM, $\text{V}{}_1\text{= 1.2}\text{mmol/min per 10}{}^{15}\text{platelets}$, $\text{K}{}_{\mathrm{<mtext>m</mtext><mtext>2</mtext>}}\text{= 46}\text{mM}$, $\text{V}{}_2\text{= 117}\text{mmol/min per 10}{}^{15}\text{platelets}$. The fact that galactose metabolites did not accumulate during the initial phase of uptake indicates that the uptake process is not mediated by enzymatic catalysis. Surface binding also appears inadequate to explain the uptake. The most likely basis for the kinetic data, therefore, is membrane transport. The kinetics are consistent with transport by coexistent membrane structures as well as with transport by a single structure manifesting negative cooperativity.