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Journal of Experimental Biology 140,107-121 (1988)
Published by Company of Biologists 1988

Inositol Transport by Hepatopancreatic Brush-Border Membrane Vesicles of the Lobster Homarus Americanus

TEVA SIU 1 and GREGORY A. AHEARN 1

1 Department of Zoology, 2538 The Mall, University of Hawaii at Manoa, Honolulu, HI 96822, USA

The mechanism of [3H]myo-inositol transport by the lobster hepatopancreas was examined using purified brush-border membrane vesicles. Transport was stimulated by a 100 mmoll-1 inward Na+ gradient, but other cation gradients were ineffective, suggesting a Na+-dependent transfer mechanism. The transport system was most efficient at pH7.0 (both sides), rather than in the presence of a pH gradient (pHin = 7.0; pHout = 5.5) or at bilaterally low pH (pHin = pHout = 5.5). The system was shown to be electrogenic in two different ways. First, myo-inositol uptake was stimulated by anions of increasing permeability (SCN- > Cl- > gluconate). Second, an outwardly directed, valinomycin-induced K+ diffusion potential (inside negative) enhanced uptake in comparison with vesicles lacking the ionophore. Myo-inositol was transported by a carrier mechanism with an apparent Kt of 0.79mmoll-1, a Jmax of 6.3pmolmg protein-1 s-1, and by apparent diffusion with a permeability coefficient of 5.92 pmolmg protein-1s-1 (mmolT1)-1. D-Glucose was a noncompetitive inhibitor of myo-inositol uptake, but myo-inositol did not significantly reduce the transport of D-[3H]glucose. Vesicles preloaded with myo-inositol trans-stimulated [3H]myo-inositol uptake, whereas those preloaded with D-glucose did not, suggesting that the inositol carrier did not transport D-glucose. It is proposed that myo-inositol does not share the glucose carrier, and that D-glucose may modulateinositol influx by binding to a ‘regulator’ site on the inositol carrier.

Key words: brush-border membrane vesicles, myo-inositol, cotransport, lobster, Homarus americanus, hepatopancreas

Accepted on June 17, 1988






© The Company of Biologists Ltd 1988