Department of Pharmaceutics (Sakurai Lab.)

Biol Trace Elem Res (2011) 142: 713-722
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 (DNP) or by sodium ion replacement. Moreover, the addition of the system N-substrate, L-glutamic acid g-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.