Enhancing Effect of Zinc on <Emphasis Type="SmallCaps">l</Emphasis>-Histidine Transport in Rat Lung Microvascular Endothelial Cells

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 ZnSO₄ (0.1 mmol/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 ZnSO₄ 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 143 mmol/L Na ⁺ + 1 mmol/L BCH. These results indicated that system-N transporter does not play a role in the uptake of l-histidine in the presence of ZnSO₄, suggesting that only system-L transporter is involved in the uptake of l-histidine, although l-histidine in the absence of ZnSO₄ 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 ZnSO₄ 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.