Apical Membrane Permeability of Mytilus Gill: Influence of Ultrastructure, Salinity and Competitive Inhibitors on Amino Acid Fluxes

Abstract

ABSTRACT The apical membrane of gill integumental cells from the mussels Mytilus edulis and M. californianus serves as a permeability barrier separating sea water from a cytoplasm rich in amino acids and other small organic molecules. Morphometric analysis of transmission electronmicrographs indicates that the membrane area of these cells is increased between 10-and 18-fold by the presence of a microvillous brush border. The microvilli do not appear to influence the kinetics of solute transport across the cell apex, as determined using a mathematical model of the relationship between membrane structure and the kinetics of transport. Rates of amino acid loss from the integument were low, and estimates of the upper limit of the passive permeability of the apical membrane to amino acids ranged from 0·5 to 10 × 10−10 cm s−1. Abrupt exposure of intact mussels or isolated gill tissue to 60 % sea water (19%o salinity) resulted in a transient, 40-to 80-fold increase in the rate of loss of all amino acids from integumental tissues. Upon exposure to full-strength sea water, efflux rates returned to near control values. Exposure to 60 % sea water also inhibited the carrier-mediated accumulation of amino acid: uptake of 0·5 μmol l−1 [l4C]alanine and [14C]taurine was reduced by 80% compared to control uptake in 100% sea water. This inhibition was not adequate to account for the increase in net efflux of taurine from gill tissue into 60% artificial sea water (ASW), though the inhibition of alanine uptake may have contributed significantly to the increased loss of this amino acid. Efflux of discrete structural classes of amino acid occurred when integumental tissues were exposed to 50 μmol l−1 concentrations of structurally related analogues. It is concluded that the apical membrane of gill cells has a very low passive permeability to amino acids, and that the overall permeability of the gill can be increased in a reversible fashion by exposure to reduced salinity or to high external concentrations of amino acid.