Enhancing Effect of Zinc on l-Histidine Transport in Rat Lung Microvascular Endothelial Cells

Abstract

The aim of this study was to examine enhancing effect of L: -histidine into cultured rat lung microvascular endothelial cells (LMECs), which constitute the gas-blood barrier. Uptake of L: -histidine into LMECs markedly increased with the addition of ZnSO(4) (0.1mmol/L), and this enhanced uptake of L: -histidine was drastically reduced in the presence of the Na(+)-independent system L substrate, 2-amino-2-norbornanecarboxylic acid (BCH). However, the uptake of L: -histidine together with ZnSO(4) was not reduced by the addition of metabolic inhibitor, 2,4-dinitrophenol, or sodium ion replacement. Moreover, the addition of the system N-substrate, L: -glutamic acid γ-monohydroxamate did not significantly decrease the uptake of L: -histidine with 143mmol/L Na (+) + 1mmol/L BCH. These results indicated that system-N transporter does not play a role in the uptake of L: -histidine in the presence of ZnSO(4), suggesting that only system-L transporter is involved in the uptake of L: -histidine, although L: -histidine in the absence of ZnSO(4) was taken up by at least two pathways of Na(+)-dependent system-N and Na(+)-independent system-L processes into rat LMECs. The uptake of L: -histidine into rat LMECs in the presence of ZnSO(4) was also found to be unaffected by pH (5.0-7.4), indicating that uptake of L: -histidine into LMECs by the addition of zinc may not be involved in the H(+)-coupled transporters.